Chapter 10 cARE OF THE CLIENTS wiry, (NDOCRINE DISORDERS introduction: The endocrine system often is consider te red as o} ee systems. es ae ree of the different Coane enon Sone is greatly i 'e function of the nervous syste: in ager : system, to coordinate _ Alterations in function of the endocrine system result in a variety of physiologic changes, which may be very serious and fatal, but at times may require minimal hospital care. The end result of most pathologic processes affecting the endocrine system is hypersecretion or hyposecretion of hormones. One of the most serious endocrine disorders is diabetes mellitus, a thronic disease which had been known since 1550 B.C. In these modem ‘mes, itis becoming a global health problem. over the world are afflicted with DM. The Todsy, mifions of people 22 life - threatening complications affecting iSease is irreversible. It causes many brain, heart, kidneys, eyes and many other organs. x i of clients with Therefore, nurses must be deeply involved pee i treatment, thus *tdocrine disorders. To afford them with adequate °O Wality life. \2mng Outcomes: My beableto. ; ‘ond ofthis Chapter, the leamer 1 Ot > abidocrine disorders clients for clinical man 577ae es ‘ogy re . . 2, Discuss tM ders nt, follow - up ca the mat i re, ; oe plan of ca for clients with endocrine oe mel: m en ol Hare to restore, maintain 2nd Promote Peat jy 4. implemen f Cm orders. i mo wth endocrine Sr comes utiized for Planning the cay 4 5. Evaluate ne disorders. the Endocrine System ‘Anatomy and PhysiolO9Y ©" Th nervous system are two of the prima, « The ine ating systems in the body. The nervous syste, communicating eheal vere impulses; the endocrine " through chemical substances known as hormones, ang 4 plays a role in reproduction, growth and development, and regulation o energy. : it tem is composed of glands or glandular tissues ; Teal eae! a secrete hormones that travel through the blood specific target cells throughout the body. A target tissue is the body tissue or organ that the hormone has its effects on. © The different endocrine glands are as follows: 4. Pituitary Gland (Hypophysis) V Lies in the sella turcica of the middle cranial fiossa (the bony floor that supports the brain). Y tt is composed of two parts: the anterior pituitary gland (adenohypophysis) and the posterior pituitary gland (neurohypophysis). Y The hypothalamus controls both the anterior and posterior pituitary S glands. And therefore, it controls the other endocrine glands. The anterior pituitary gland hormones and their functions are & follows: a. Growth hormone (GH). It is also ki ee i . nown as somatotropin somatotropic hormone (STH) " * Itis concerned with fi growth of cells, bones and soft tissues * Itaffect 5 th carbohydrate, protein and fat metabolism. Ute e282S blood glucose levels by reducing gue b. Prolacin Pann insulin antagonist. lactotonic ee, tt {8 also called _mammotropic Lai © Hig one, OF luteotropic hormone. 578,. Go! : Gonadotropi » The two gonadotropins are: folie — stimulat; (FSH), and luteinizing hormone (LH) stimulating hormone » They affect ‘development of seco ndary sex characterist They ecessary fo * ristics. production in males and fora oeness and sex steroid e. Adrenocorticotropic hormone (ACTH) or Adi i » Itcontrols functions of the adrenal anata f Nelanoys 7 aa hormone (MSH). . » It is necessary for pigmentati oa i 7 enithelial pigment layen no 8 skin, retina (melanin y The posterior Pituitary gland hormones and their functions are a. Antidiuretic hormone (ADH). It is also called vasopressin. + It is the major contro! of osmolality (concentration) and body water volume. « It increases water reabsorption in the collecting ducts of the kidneys. * It causes vasoconstriction. b. Oxytocin. «It promotes milk "let - down" in a lactating breast. * It causes increased uterine contraction after labor has begun. 2. Thyroid Gland. Y The thyroid gland hormones are as follows: « Triiodothyronine (Ts) , Thyroxine (T. "4). These two hormones: * Regulate metabolic rate of cells. * Regulate protein, fat and carbohydrate metabolism. * Actas insulin antagonists. * Maintain growth hormone maturation. " Affect central nervous systems (CNS) development. "Affect cardiac rate, force and output. * Affect oxygen utilization. i " Stimulate lipid turnover, free fatty acid release and cholesterol synthesis. ae "Stimulate sympathetic nervous system (SNS) activity. * Thyrocalcitonin (Calcitonin). " ‘Itlowers serum calcium levels. * Itinhibits osteoclastic sci * Itlowers phosphate lever. absorption in the G.l. * Itdecreases calcium and phosphorous tract. secretion and promote skeletal 579Icitor i 2 . enn aes inverse: aoe high, Calcium is (+) low 7 Tryrocaletor 7 } Mey Calcium is (1) high ° 3. Adrenal G20 rahe adrenal gland are the cortex and medu ote Hf hormones control the "3S: Sugar, ‘Salt and ro cocorticoids (Cortisol) 7 coctn ood glucose levels (Sugar). : = Enhance $I wyconeogenesis (protein catabolism and fat catabolism li is). = Have anti-inflammatory effect. : = Decrease phocyte participation in cell-mediated immunity immunosuppressan). « Decrease new antibody release. = Increase gastric acid and pepsin G.L. irritation. = Maintain emotional stability. 2. Mineralocorticoids (eg. Aldosterone) = Maintain sodium and volume status (Salt). «Increase sodium reabsorption in distal tubules of the kidneys. . jelersd @ Passi nr excretion in distal tubules. . isp ium,” “anti- sium." (Aldosterone retains sodium, excretes potassium). Increased aldosterone level results to: Hypernatremia Hypokalemia a heated Peciemcdo level results to: 2. SexHorvonse (and . Sex Hormones (Androgen Responsible for re Estrogen) 7 females. In males reiceceay sex characteristics steroids. , hormones work like gonad! The adi ang Adrenal medulla secretes catecholamines (epinephie production. This may cause Norepinephrit : conga rine) through stimulation of the SNS and mee 7 effects of s) stimulation 2 YmPatho-adreno-medullary response (saw?) function fs hightone ogan® are as Tullos: (concest and fast, except G. and G.U.") 580j ea Dilatati lerines estecsnoaa . | es peace Of pupils; relaxation of ciliary Relaxation of bronchial ee Lungs (bronchodilatation); increased muscles Decreased saliv; i th ary glands secretion; > Mou dry mouth and thirst a See Gastrointestinal Tract Decreased production of GI secretions; i. decreased motility and contraction of sphincter E Urinary Bladder Relaxation of detrusor muscles and contraction of sphincter (urinary retention) ah + Pancreas Decreased secretion of Islet cells; decreased insulin secretion; increased serum glucose levels. + Fat cells ~ Lipolysis a ine functions of the * The Islets of Langerhans perform the endocrine functio Pancreas. It has 2 types of cells, the alpha cells and a The |, ‘pha cells secrete glucagon; while the beta cells secrete i i | Slucagon enhances gluconeogenesis (breakdown - ce Proteins, into glucose) and elevates blood glucose levels. "sulin produces the following effects: Liver calls ; Increase glycogenesis. | © Ncreased fatty acid synthesis. gluconeogenesis, and Decreased lycogenolysis, > agt@togenesis, Ail : ae tissues * increased fatty acid synthesis.juscles is. 7 : 2 " increased alycoge ne uptake and protein synthesis, b Increases Sryotein catabolism. c. Decre’ hysiologic changes in the endocrine system associated with ating v Thepl | oe ovarian functioning resulting in changes in reproducing and sexual Sens hypothalamic hormones _ influences . Neatneas to changes in the intemal environment and to rs. . Decreased levels of prolactin, growth hormone. * Increased levels of ADH; however alterations in Fenal function decrease ability of the elderly to concentrate urine and hyponatremia can result; nocturia is also commonly present. * Hypothyroidism occurs due to changes in thyroid gland structure. * Decreased vitamin D levels, negative calcium balance, bone loss, decreased intestinal adaptation to varied calcium intake. * Renin - aldosterone response to postural changes and volume depletion is depressed. The client is at risk to postural hypotension. * Impaired glucose tolerance due to delayed glucose - induced insulin secretion, altered hepatic handling of glucose and impaired insulin - mediated glucose uptake. Non - insulin - dependent diabetes mellitus (NIDDM) is one of the more common chronic diseases ‘among the elderly. * Decrease in size of the liver. se in enzymes involved in the metabolism with duss Increased Propensity to drug toxicity. . Parathyroid Glands "Produce par * PTH regulates * PTH elevates bones, calcit aaa ‘um and phosphorous balance Serum calcium levels by withdrawal of calcium f° Low serum calci : The rltonaip ore stimulate PTH release ; and calcium is dj ae "Persecretion of PTH: eam is — proportion. 582retion of PTH. ia . PTH elevates serum calcu osPhatemia phosphorous levels vels and inversely, lowers tic Tests of Thyroid Disorders 089 roid Function Tests a. Thyroid - stimulating hormone assay +: Hypofunction of thyroid land; pri fe ‘J; Pituitary disorders; hyperthyrenien hspethyrokdism, bp. Radioactive lodine Uptake (RAtU) *: Hyperthyroidism; urine: hypothyroidism J: Hypothyroidism; urine: hyperthyroidism. = Patient Teaching: o Radioactive dose is small and harmless. o Contraindicated in pregnancy. o Seafoods may elevate results. o Drugs that may elevate results: barbiturates, estrogen, lithium, phenothiazines. Drugs that may decrease results: Lugol's solution, saturated solution of potassium iodide (SSKI), antithyroid, cortisone, aspirin, antihistamines. o Collect 24-hour urine specimen after oral tracer dose given. o Thyroid is scanned after24 hours. ° c. Thyroid antibodies : t: Thyroiditis d. T3:T, Radioimmunoassay THyperthyroidism Hypothyroidism €. Free Thyroxine Concentration Ts Resin Uptake Thyroid Binding Globulins te Hyperthyroidism +: Hypothyroidism ” Diagnostic imaging Studies 3. Thyroid Scan - dose is harmless. {Radioactive iodine taken oral dose is ha * Scanning done after 24 hours ications. " Avoid iodine containing foods; dyes: bias “ Cold nodules: cancer 583prepa ition No 9 Imaging Resonance nag clients with metal implants ¢ 4, for allergy I Tomograpny histor ‘ Contcontrast medium is used, note allergy history. > piagnostc Tests of Parathyroid Disorders a. Total serum calcium = Venous blood is collected et Hyperparathyroidiom et Hypoparathyroi ism i b. Qualitative Urinary Calcium (Sulkowitch Test) * Collect urine specimen. = Fine white precipitate added to urine specimen. ao = Absent or decreased precipitate indicates low serum calcium ang hypoparathyroidism. c. Quantitative Urinary Calcium (Calcium Deprivation Test) = Collect 24 - hour urine specimen. = 1: Hyperparathyroidism = J: Hypoparathyroidism d. Serum Phosphorous * Collect venous blood specimen. * +: Hypoparathyroidism = J: Hyperparathyroidism e. Serum Alkaline Phosphatase = Collect venous blood specimen. + 1: Hyperparathyroidism 1c 4: Hypoparathyroidism | Parathormone (PTH) Radioi : ne venous blood pny, : faceeain most specific test for heme on wth serum calcium levels, this is #? 3. Diag 'yperparathyroidism : nostic Test : a. Cortisol a wah genccontical Disorders ve dexamethasone asone Suppression test jormation of ACTH” Pefore phlebotomy to suppress should form when Sulkowitch reagent is du : Pituitar ry tumor, Cushing's nde es 584| b ¢ | | 4 | . Addison's disease. ¢ : een level 0" fasting is required; the patient pefore the test because activity pee On bed rest t, Cushing's disease. Cortisol level * |: Addison's disease. 1- hydroxysteroids . 24 hour urine collection to be ; , ft: Cushing's disease. Kept on ice . 4, Addison's disease. I- ketosteroids + 24hour urine test; keep collection i . t:Cushing's disease. Cold; may need preservative + 4: Hypofunction of adrenal gland for 2 hours piagnostic Tests of Adrenal Medullary Disorders b. Vanillylmandelic Acid Test (VMA. Test) * VMA is a metabolite of epinephrine. * 24 hour urine specimen is collected. * Instruct the client to avoid the followi may alter the result: o Coffee o Chocolate o Tea o Bananas o Vanilla o Aspirin * Normal Value: 0.7 - 6.8 mg/ 24hr. Total Plasma Catecholamine Concentration * The client should lie supine and rest for 30 minutes. * Butterfly needle is inserted 30 minutes before blood specimen is collected (to prevent elevation of catecholamine levels by the stress of venipuncture). Normal values: OWL) © Epinephrine: 100 pg/ml (590 pm © Norepinephrine: 100 to 550 pd/ml (590-3240 pmol/L) Clonidine Suppression Test : 5 © Clonidine (Catapress), a reece adrenergic blocker Suppresses the release of catecholamines. a ° In piescience ana) clonidine does not suppress the Of catecholamines. it | dose of ° Nomal Response: 2 to 3 hours after a single eae Clonidine, the total plasma catecholamine value decreases =t least 40% from the client's baseline. 585 ing medications and foods which5. Diagnostic Tests Ultrasound + CT Scan, MRI and Uhre mocytoma. 6. To localize the pheoct Disorders (Diabetes Mellitus) : of Pancreat. °3G (Fasting Blood Glucose): 7 ; FBG a. FBS (Fasting Blood Sugar = Normal: 70-1 oe readings. = DM: 140 mg/dl a Bh b, 2-hour PPBS (2+. Posprandial Blood Sugar) . a men is jrawn. «I carbohydrate in det is taken by the client + 2 hours after meal, blood specimen Is withdrawn: bloog Sg returns to normal level. ¢. OGTT/GTT (Oral Glucose Tolerance Test/ Glucose Tolerance Test) ‘Take high carbohydrate diet (200 to 300 g.) for 3 days. ‘Avoid alcohol, coffee and smoking for 36 hours before the test NPO for 10 to 16 hours. Initial blood and urine specimen are collected. 450 to 300 g. of glucose per orem or IV is given. Series of blood specimen is collected after administration Of glucose (30 mins., 1 hour, 2 hours, if required 3 hours, 4 hours, after). and 5 hours lf glucose levels peak at higher than normal at 1, and 2 hours af. en ae injection ef glucose, and are slower than normal to turn to fasting levels, then DM (diabetes mellitus) i Done when results of FBS and 2- hss) Fe confirmed, normal). hour PPBS are borderline (bigh 4. Glycosylated Hgb (HbAic) * Most accurate indicator of Reflects serum glucose Normal value is 4% to 6' The goal for the client DM (diabetes mellitus). levels for the past 3 to 4 months. % (up to 7%) for nondiabetics. with DM is 7.5% or less Excess glucose in the blood Attaches to hemoglobin (hgb) Hgb (com ponent of rbc} Lifespan is 90~ 129 dave 586sine Disorders pt" rs of the Pituitary Gland ior Pituitary Gland (A ' 1 Ath Hormone (ont enophyats) 4. Gigantism. Is hypersecretio i befor epiphyseal Closure). This ‘cna ie Ge! i exaggerated growth in height and ‘ight iene i 2. Acromegaly. Is hypersecretion of ony closure). This is caused Primarily by itu manifestations are: ts ugh pa rbances; arthritic : ning of Voice in; hypertension; dysphagia; 3. Dwarfism. Is hyposecretion of is i i pow la hoe. GH. Itis characterized by failure to ¥ Prolactin (Mammotropic, Lactotroy 4. Galactorthea. Is hypersecreti excessive milk production. 2. Absence of milk production during Jactation results from hyposecretion of prolactin. opic, Luteotropic Hormone) lion of prolactin. It is characterized by ¥ Adrenocorticotropic Hormone (ACTH) 1. Secondary Cushing's Disease. Is hypersecretion d ACTH. 2. Secondary Addison's Disease, Is hyposecretion of ACTH. ¥ Thyroid - Stimulating Hormone (TSH) 1. Secondary Hyperthyroidism. Is hypersecretion of TSH. 2. Secondary Hypothyroidism. Is hyposecretion of TSH. Y Gonadotropins (FSH and LH) : 1. Hypersecretion of hormones results to precocious puberty. 2. Hyposecretion of the hormones results to failure_to_develop Secondary sex characteristics that normally develop at the age of Puberty. The manifestations are as follows: Males Females i breast * Small phallus and testicles °_Failure to develop bers | * No growth of body hair . Soe ai ly | * Decreased libido E . lation : Im ce - 5 Aone = Infertility 587ze appea! fi : 1 tap eternal tar = Seca) results to albinism ( (hypopigmentay 2 of the eons character2e A ifculy “in ee pioment of fmesence of bright Fight ing daytime ; nd (Neurohypophysis) . Posterior DH) ; 7 ‘Antidiuretic iobey fe Ponmone is Syndrome of Inappropriate ntidiuretic Ho! ae . * ‘Causes include trauma, stroke, Ussinealati 7 sites SIADH is characterized by excessive ntion re ety oe triatic manifestations of SIADH are as follows; . 4. Edema, weight gain. This is due to excessive retention ter. sage 2. \acieneion. Vasopressin causes vasoconstriction. 3. Dilutional hyponatremia. This is due to excessive retention of water, without proportionate retention of sodium. * Collaborative management for SIADH include the following: 4. Administer diuretics as prescribed to reduce body fluids. 2. Administer Demeclocyline (Declomycin) as prescribed. tt inhibits ADH - induced water reabsorption and produces water diuresis. 3. Restrict fluid intake as prescribed. 4. Monitor VS, cardiac and neurologic status. Water intoxication may cause CHF and increase in ICP. 5. Monitor | and O, daily weight, electrolyte levels. : Hyposecretion of ADH is Diabetes Insipidus (D.I.). * Diabetes insipidus is characterized by inability of the renal tubules 10 Leal water (water loss). e most characteristic, manifestati is i ch as 20 L of urinelday), tation of D.I. is polyuria (as mu * The urine is diluted or water- like, wi i i : Ales - like, with low specific gravity. on manifestations of D.l. are as follows: polydipsia, dehy4 © The ton, retarded growth in children diagnostic test for D.. is ids withheld for 4 to 18 hours. if ; . re Confirms presence of D.I 1 opresenomones used in diabetes insipidus are as follo** cetate (DDAVP, Stimate) 588 ration,2. Vasopressin (Pitressin) _Gapeate as aire tn cot in + Chlorproprat (Diabenese) and thiazide A action of vasopressin. diuretics. potentiate the _—____ GOMPARISON BETWEEN SIADH and bi it conceP 4, ADH (Antidiuretic hormo Retains water )! Vasopressin Vasoconstriction (elev; 2. SIADH: Water tenon a) Low serum Na* 3._D.I. : Water loss ‘SIADH DE. | me of Inappropriate ADH) (Diabetes insipidus) iv Hypersecretion of ADH © — Hyposecretion of ADH ||, Water retention / water inside the |» Water loss / water outside the | body (in the blood) body (in the urine) ||, Low serum sodium (dilutional | High serum sodium hyponatremia) Decreased urine output (oliguria) Increased urine output (polyuria) Increased urine specific gravity / Decreased urine specific gravity / | | osmolarity (concentrated urine) osmolarity (dilute urine) | |» Decreased blood —_ osmolarity Increased blood ~— osmolarity (hemodilution) (hemoconcentration) © Constipation « Growth retardation * Treatment: Diuretics e Treatment: Desmopressin, L Pitressin Laereenlnr jituitary hormones. * Is hyperfunction of the anterior pi t t * Its frequently caused by benign pituitary adenoma; may result also fom i ituitary tissues. . Pe eras ot ti secreting tumors) account for 60 to 80% of all : The charac tovitic manifestations of hyperpituitarism are as follows: io in acromega! 1. Overproduction of growth hormone ee adults; gigantism in children. 2. Hormonal imbalances. 3. Neurologic manifestations: 589° ° 4, Endocrine manifestatio ° ° ° ° ° , or scotomas (blind spots In the visual fois. ae ,ased intracranial pressy is of increé i le som and sy roogic Disorders) Chapt izures. 8 fora oh noetie. seep. temperature regulati a ape to hypothalamic involvement ation et corfirm presence of tumor: skull X-ray, cy ic scan, MRI (rey ns: ; ; novulatory periods, oligomenorthea, (scanty Iregular mS orrhea (absence of menstrual flow). menstrual flow), amen Infertility 7 oduction) intercourse), vaginal mucosa atrophy, decreased vaginal lubrication, decreased libido due to in steroid effect. : Decreased libido and impotence, reduced sperm count, infertility and gynecomastia in males. : = The collaborative management for hyperpituitarism are as follows: 4. Surgery: Transphenoidal hypophysectomy ° ° ° Hypophysectomy is surgical removal of the pituitary gland. The incision in transphenoidal hypophysectomy is made between the upper lip and upper gum. The nursing interventions after transphenoidal hypophysedomy are as follows: ~ Keep head of bed elevated, at least for 2 weeks. To promote venous drainage and drainage from the surgical site. ~ Maintain nasal packing in place and reinforce as needed. ~ Provide frequent oral care with toothettes. To prevent trauma to the incision. Instruct client to avoid blowin: ivities thal i: 2 a ig the nose and activities lente Pressure (ICP). ~ indinane Of 20 postnasal drip or nasal drainage which might indi inage drainene oik29° of cerebrospinal fluid (CSF). Check nes! Rast Hari CSF is positive for glucose. . O en vein, Outputs above 900 mis/ 2 hours oF urine insipidve, below 1.004. These indicate diabel® Adminis ie as Presciag, amooks and other hormone roles ormone (soma: ay i in, (somatotropin), 'y include vasopress' 590Radiation therapy as prescribe . pharmacotherapy. i o Parlodel (Bromocriptine) to lower | Hand pypoitultarism Heat 17 Is rypofunction of anterior pituitary gland caus pituitary hon Dea and the hormones ene deficiencies in both cause: as follows: tumors, trauma, the target glands. joke, Surgery OF radiation of pituitary gland encephalitis, autoimmunity, The clinical manifestations of inypomun . Mild to moderate obesity (low GH Fee are as follows: Reduced cardiac output (low GH. ‘ADH. Infertility, sexual dysfunction (low Fatigue, low BP. (low gonadotropins, ACTH) Headache, hemianopsia (due t f gland is located near the optic pico Of the. pitukary gland; the v The collaborative management for h popi is » Surgical removal of the tumor. Eee eee » Radiation therapy. « Hormonal replacement therapy (HRT). < epacge simmond's Disease ¥ Is panhypopituitarism. It is total absence of all pituitary hormones. Sheehan's Syndrome 7 Is hypopituitarism caused by postpartum pituitary necrosis. ¥ ltoccurs in women with severe bleeding, resulting to hypovolemia and hypotension at the time of delivery. Disorders of the Thyroid Gland * Goiter is an enlargement of the thyroid gland ¥ This is due to increased amount of TSH. I hyperthyroidism, hypothyroidism or euthyroidism. It can be associated with Hyperthyroidism. Is hypersecretion of thyroid hormones. i A common cause iw Brave's disease, also known as toxic diffuse goiter. ¥ Incidence is higher in females, below 40 years 20°. ondary with ” Itis primarily associated with severe emotional 3 autoimmune disorders. He hased on 3 Basi The clinical manifestations of hyperthyroidism are 3 Basic : ypersecretion of Ts). * Increased metabolic rate (due t© MYPETT ersecretion of 4) ‘Increased body heat production (¢ wn of tyrocaleitonin)- Hypocalcemia (due to hypers@ 591enhance _the — actions — of —poinenhrine ang : 0 ic activity and cer v Tnyroid poor nereasing sympathetic activity ntral nervous ction. increased cell membrane permeability >). « Resear neal ay "Th leads to increased Nett oF hyperthyroidism are as follows: v The clinical mane = Thyroidal dist functions: 2 SNS and CNS functions: = a Sena nervousness, irritability, agitation o Fine tremors o Tachycardia o Hypertension o Diaphoresis b. Increased metabolism © Increased appetite to eat o Weight loss o Heat intolerance c. Hypocalcemia o Diarthea (increased peristalsis) o Fine, silky hair o Pliable nails d. Altered reproductive function o Amenorrhea * Ophthalmopathy a. Exophthalmos. Is protrusion of the eyeballs. This is caused by accumulation of fluids at the fatpads behind the eyeballs, pushing the eyeballs forward. This may cause corneal ulceration, Q sphere, a haphctrtey Exophthalmos is irreversible. | a Graefe's ,sign (lid lag). Long and all I fissure is sill evident wien one looks down oa a Dae cnn forehead Temains smooth when one looks up. 7 8S sign (Thyroid stare). Is characteri: right : omnes infrequent blinking. , a e ¥. This is manifested by warm, flushed, sweaty skin, and thickened, hyperpigmented skin at the pretibial area, i | Basle Concepts to Remember in Hyperthyroidism L ig ns and Symptoms are based on the following Concepts: | 1" is fast: hypertension, ” "Eg. high and fe lon, tachycadi ae wet: diaphoresis (wet skin), diarthea rf pal oh Le iain S92ll z ‘Eve manifestations.” E.g. 3. collaborative management fo; Provide adequate rest. Provide non - stimulating, quiet agitation and heat intolerance. stare. Sxophthalmos, tid lag, bright — eyed “Hypocalcemia” hyperthyroidism are as follows: and cool environment. To prevent provide high- calorie diet. To maintai a Low- fiber diet, if with diarhea Nona! status Obtain daily weight. This is the best indicator of nutritional status. Promote safety. The client is at high risk for injury due to restlessness, nervousness, agitation and tremors. fe Aa Ad Mile exophthalmos. Instill artificial tears at regular . Advise client to wear dark i out under the sun. sre ecard ate Avoid stimulants like caffeine. Replace fluid electrolyte losses due to diarrhea and diaphoresis. Pharmacotherapy in hyperthyroidism: ° Anti- thyroid medications lodides: Lugol's Solution and Saturated Solution of Potassium lodide (SSKI). 1. Inhibit release of thyroid hormones. 2. Mix with water or fruit juice with ice to improve palatability. 3. Provide drinking straw to prevent permanent staining of teeth. 4. Side effects: (lodism) allergic reaction, metallic or brassy taste in the mouth, increased salivation, coryza, vomiting, abdominal pain, rash, sore gums. i ; Thioamides: Tapazole (Methimazole), PTU (Propyithiouracil) 1. Inhibit synthesis of thyroid hormones. SHH : 2. Side effects: ‘Agranulocytopenia: Neutropenia with leukopenia (manifested by fever, sore throat, skin rash, diarrhea). When antithyroid medications are given: ‘ 1. Monitor vital signs (especially BP and pulse tat oe Tse nestor eee geen Weight gain indicates M . Administer with meals to avo ee containing iodine. ASA . Avoid ASA (Aspirin) and ‘ovels; iodine- containing elevates free thyroid hormone A ang antagonize medications stimulate thyroid antithyroid medications. - on 593axe ont 10 conaut PRYSICaN before eating iodized a, : jit ich foods. — ene itor ie and symptoms of hypothyroidism, 7 Inderal (Propranolol) : Bete Do ia and hypertension thasone [0 cont anne! blockers, dexame’ 7 carrnibR i action of thyroid hormones. joactive lodine (hist) i tion for few days. Body secretions Use gloves when handling = Radiation Therapy: — : Place client on iso Ps 7 radioactve- contaminated. body nt women because of potential teratogeni, on nat b ae Paspraney should be delayed tor 6 months after therapy. «= Surgery: Subtotal Thyroidectomy (5/6 of the gland is removed). a. Care of the Client Undergoing Thyroidectomy © Preoperative Interventions 1. Promote euthyroid state - Obtain VS and weight. Ensure VS are stable. - Assess electrolyte levels. - Assess for hyperglycemia and glucosuria. - Thyroid hormones act as insulin antagonists. 2. Instruct client on how to perform DBCT (deep breathing, coughing and turning) exercises and how to support the neck 7 na the ana eet ley when coughing and moving. . Administer the jing medicatic il Pvielpireds 9 ications as prescribed to prevent - Sodium lodide Solution (Lugol’s Solutions). To reduce the size and vascularity of the thyroid gland and prevent : eo ore on an thyroid crisis. tctyearda, ) to control hypertension and - Gl rah fea tyro Poets (€.9. dexamethasone) to inhibit acon o * damage resuts fone” (ECG). Heart failure or cardae P sion and tachycardia. © Postoperati 1. Poatton Interventions: i ~ Fowler's wi Grect. Hy owler’s with head, shoulders ‘on YPetextension or flexion ef oe oe va back of the nat the back of the neck Bioed may now 0 ¥ Gravity. Respiratory distress may indica? 594bleeding. Accumulati airways. lation of blood in the neck 3. Have tracheostomy set, oxyge, may compress 7 : a 7 bedside. Inadvertent parathyroid gut, avaiable atthe iia eo Hypocalcemia ine a damage leads to , to airway ob: i use fay 4, Assess for recurrent lane Fyngospasm that - Ask client to speak Hest Nerve dai name.” Ty hour, e.g., - Limit client talkin, Mild hoarseness is panes level of hoarseness. induction of an ‘anesthoste beled to intubation during laryngeal nerve damage. ‘Notiy te ees indicates - Observe for other signs of Physician. damage like respiratory ob: enone laryngeal nerve pitched voice, stri struction, dysphonia, high - : ice, stridor, dysphagia and restles: 5. Monitor for signs of hypocalcemia and ea eee due to trauma of the parathyroid gland. iny. This may be - Keep Calcium glucon: ily avail - Monitor blood Press to teuele tx Peale Ton oats sign (carpal spasm) which indicates hypocalcemia. (Compression of the brachial artery with BP cuff for 3 minutes is done to assess for Trousseau's sign). - The other signs of tetany are as follows: > Cardiac dysrhythmias Dysphagia Muscle and abdominal cramps Numbness and tingling of the face and extremities Positive Chvostek’s sign Seizures Photophobia Wheezing and dyspnea (due to spasm of the airways) 6. Monitor for thyroid storm , 7 - Thyroid storm is fect and potentially life threatening hyperthyroidism. ; - threatening Myo release of id hormone into the bloodstream during surgery; t can also follow severe it i stress. i i infos ae cnank tions of thyroid storm area as ae (elevated temperature). This is the initial sign of thyroid storm. > Tachycardia, dysrhythmias: > Systolic hypertension. 595 “will you state your VVVVVVV‘cogtations: nausea and vomiting, diay > Glmani tation, imitability, anxiety, tre, ness, ag! . * tremor, > Restless! seizures. , nn ind coma. > Delaborative management of thyroid storm are ag pat say ond SRE ey (oxygen therapy). ister a id medications (PTU, sod 7 ce solution (Lugol's solution), Inderal (Propranoigy and glucocorticoids (dexamethasone) as prescribed, > Monitor VS, | and O (intake and output), neurologic status, cardiovascular status every hour. > Implement measures to lower fever. Use cooling blanket. Administer acetaminophen as prescribed. Avoid ASA, Salicylates increase free thyroid hormone levels. > Maintain quiet, calm, cool, private environment until crisis is over. . Patient teachings after thyroidectomy include the following - Support neck with interlaced fingers when getting up from bed to prevent hyperextension of the neck. - Start range-of-motion (ROM) exercises of the neck 3 to 4 days after discharge. - Massage incision site with cocoa butter lotion, once healing occurs. To minimize scarring. - Have regular follow - up check-up. Summary of Potential Complications of Thyroidectomy Hemorrhage Airway obstruction Tetany Recurrent Laryngeal Nerve Damage Thyroid crisis (Thyroid Storm, Thyrotoxicosis) Myxedema (Hypothyroidisrn) KAA N < * Hypoth i P Aanyroidism. |s deficiency of the thyroid hormones. ¥ The causes of hreg? odism in adults; cretinis in children. 's hypoth 'ypothyroidism are as follows: 596x i disorders (e, ir 1, Autor associated with nee ron acase an auto’ ford < recurrent respi ; ione) utoimmune Radioactive lodine (I;3;) therapy AntithyroKd Or ta Jinical manifestations i TH cancapt of hypothyroidism are based on 3 7 Decreased metabolic rate (due to hy 2 Decreased body heat production (due to hy 3, Hypercalcemia (due to hyposecretion of thyrocalcitonin) «Hypercalcemia results to decreased cell membrane permeabili This leads to decreased Neuromuscular irritability. ies ey The clinical manifestations of hypothyroidism are 22 follows: 2. 3. ion of Ts). yposecretion of T,) 4, Slowed physical and mental reactions. 2. Apathy, lethargy, fatigue. 3. Weakness, muscle aches, paresthesias. 4, Dull, expressionless, mask- like face. 5. Cold intolerance; subnormal body temperature. 6. Generalized puffiness and edema around the eyes and face. 7. Anorexia. 8. Obesity or weight gain. 9. Bradycardia. 10. Constipation. 11.Coarse, dry, sparse hair, loss of body hair. 12.Dry skin, brittle nails. 13.Cardiac enlargement, tendency to develop congestive heart failure. 14. Hyperlipidemia, atherosclerosis. 15.Forgetfulness and loss of memory. 7 Slow speech: husky hoarse voice. -Enlarged jue. 18. Increased ee arty to sedatives, narcotic and anesthetics. Basic Concepts to ember in Hypothyroidism Signs and Symptoms are based on the following Concepts: 1. “Everything is low, slow and dry.” eg, Low and Siow. slowed physical and mental reactions, lethargy, low body temperature, bradycardia, Slow sn atic !) Ory. dry hair, nails and skin, constipation (ary stool) 5972. Hypercalcemia | borative management for hypothyroidism ar v er VS. Tyonnlert for changes in heart rate and rhythm indicate cardiovascular disorders. \ Wich | : Saline: 2 Note calorie, IW celeste, ow-saturated fat 1g | it hyperiipi ia. ; 4. nese the alent for constipation. Provide high fiber/ Toughage adequate fluids to prevent constipation. and 5. Administer thyroid replacement therapy: * Synthroid, Levothroid, Levoxyl (Levothyroxine) = Cytomel(Liothyronine) = Thyrolar (Liotrix) = Thycar (Thyroid)' ¥ Nursing Interventions in Thyroid Replacement Therapy 1, Monitor VS, especially BP and pulse rate. Hold medication for hig, blood pressure and tachycardia. Notify physician. 2. Monitor weight. Reduction in weight is desirable. 3. Instruct client to take the medication in the morning without food. To ensure absorption of the medication. 4. Instruct client to avoid foods that can inhibit thyroid secretion such as strawberries, peaches, pears, cabbage, turnips, spinach, Brussel sprouts, cauliflower, radishes and peas. 5. Start with low dose, then gradually increase as prescribed by the Physician. To prevent hyperthyroidism or thyroid crisis. 6. Advise client to report signs of hyperthyroidism like tachycardia, chest pain, palpitations and excessive sweating. 7. Thyroid hormones have the following drug interactions. 7 * Enhance the action of oral anticoagulants, sympathomimetics and anti- depressants, | . a the action of insulin, oral hypoglycemic agents a4 igitalis. ‘ P a of rp hormone is decreased by Dilantin (Phen egretol (Carbamazepine). 8. Thyroid hormones should Se auel at least four hours apart fe These dant antec, bile acid sequestrants, iron and : ‘ecrease the absorption of thyroid replacement ¥ Myxedemic Coma. ser eo na. Is extreme, severe stage of hypothyroidism. " Ca i n be Precipitated by acute illness, rapid aoe and narcotic" "°5!. Surgery, hypothermia, or us? 598clinical manifesta i Tyypotension tions of myxedomic coma are 2. Bradycardia as follows: 3, Hypothermia 4, Hypoglycemia 5. Hyponatremia 6. Respiratory failure 7. Coma | Signs are profound! tentially fatal 7 . gen management for myxedemic coma are as 4. Maintain patent airway. 2. Administer IV fluids and Synthroid/lV as prescribed. 3. Administer glucose/IV as ordered. 4. Monitor client's temperature. Correct hypothermia. Keep client warm. 5. Monitor BP. Manage hypotension. 6. Monitor for changes in level of consciousness (LOC). 7. Monitor for electrolytes and glucose levels. Correct hyponatremia and hypoglycemia. Disorders of the Parathyroid Glands 1, Hypoparathyroidism. Is hyposecretion of parathormone (PTH). Y Hypoparathyroidism can occur following thyroidectomy because of temoval of parathyroid tissues. ” The clinical manifestations of hypo! 1. Hypocalcemia and hyperphosphatem2 ‘Neuromuscular excitability. 2. Signs of tetany: * Cardiac dysrhythmias Carpopedal spasm Dysphagia Muscle and abdominal crampé and extremities Numbness and tingling of the face Positive Chvostek’s sig) Positive Trousseau's sig" Seizures : Visual disturbances (photophobia) n, laryngospas™) Wheezing 2nd dyspnea (bron 'ypotensic~ parathyroidism are as follows: ia. Hypocalcemia increases Hi 3. 5994. The collaborative management for hypoparathyroidisn, follows: en NOE 2 ‘Anxiety, irritability, depression are a itor VS. Notify physician for hypotension Moonee for signs of hypocalcemia and tetany. Place client on seizure precaution. : ; Have tracheostomy set, oxygen and suction available at These are emergency equipment to be used for spasm of ai Administer calcium gluconate/ IV for hypocalcemia. Diet. High-calcium, low-phosphorous diet. IWays, Administer phosphate - binder (amphogel) as prescribed. To lower phosphorous level and increase serum calcium level. . Administer calcium supplement and vitamin D as Vitamin D enhances calcium absorption from the G.I. tract. Calcium Supplements - Calcium Carbonate (BioCal, Caltrate 600, Rolaids, Tums) - Calcium Carbonate - oyster - shell derived (OsCal 500, Oysco, Oystcal) Calcium citrate (Citracal) - Calcium glubionate (Calcionate, Neo - Calglucon) - Calcium gluconate - Calcium lactate - Dibasic calcium phosphate - Tribasic calcium phosphate Vitamin D Supplements - Calciferol (Calderol) - Calcitriol (Calcijex, Rocatrol) - _Dihydrotachysterol (DHT, Hytakerol) - Ergocalciferol (Calciferol, Drisdol) Calcium Regulators - Alendronate (Fosamax) - Calcitonin human (Cibacalcin) Calcitonin salmon (Calcimar, Miacalcin) ~ Etidronate (Didronel) - Pamidronate (Aredia) - Pisedronate (Actonel) : Tiludronate(Skelid) il oun Salts with Digoxin increase risk of digoxin tose ral Calcium salts reduce the absorption of T aaGerclum regulators (eg. Fosamax should be taken with wane? Should ater not, be Thesast and to remain upright for a least 30 minute: chewed. pp prevent gastroesophageal rey,“ '°88t 30 minutos. The rparathyroidism. Is hypersecretion 1 "Eris results to high serum calcium Teveparathormone (PTH) The clinical manifestations of hyperparathn pone demineralization 1. Hypercalcemia and hypophosphaters om © a8 follows: neuromuscular excitability, “¥percalcemia decreases Fatigue and muscle weakness, Skeletal pain and tenderness, Bone deformities that result in Anorexia, nausea, vomiting, ey Weight loss. . Constipation. Hypertension. ). Cardiac dysrhythmias. 40.Renal stone. bh collaborative management for hyperparathyroidism are as lows: . Monitor VS, particularly the BP. Hypertension may occur (calcium promotes vasoconstriction). . Monitor for cardiac dysrhythmias. . Monitor for urine output. Polyuria causes dehydration. Monitor signs of renal stones (calcium stones). ; . Move client slowly and carefully. He may experience skeletal pain and he is at risk to develop fracture. ; Increase fluid intake. To prevent dehydration and renal stone formation. 7 . Administer Lasix (Furosemide) as prescribed to lower serum calcium levels. i intain hydration. 8. Administer Normal Saline/IV as prescribed to maintain hyd Sodium enhances excretion of calcium. crease skeletal 8. Administer calcitonin (Calcimar) BT Jearance of calcium. calcium release and increase rena! oe : 10. Administer antihypercalcemic as Pre 1 Ago nitrate (Ganite) rescribed. -Administer phosphates as P' Is. i Monitor calcium and phosphorous love pr ‘arathyroidectomy rathyroid glanc® Y Removal of one or more of the Pa Pathological fractures, Pigastric pain. PENeaPoen « aren = ~ 2 601postoperative Cae respiratory distress. : 7 Pos ontor fOr FESPIT Es oxygen and suction at the beds Have bedside, Vital Signs ee et Monto fo bleescacemic crisis (signs and symptoms y 9 tetany ater calcium supplement and vitamin D as prescr seacce Disor f the Pancreas - 1 reine Mellitus. Is @ chronic disorder of carbohydrate, fat and metabolism: ee E - ; Protein Y It is due to inadequate insulin production or increased resistance to v v Insult ge of DM is unknown The cause s ? : The predisposing factors to DM are as follows: : | : a. Stress. It stimulates secretion of epinephrine, norepinephrine and glucocorticoids. These hormones elevate blood glucose levels by glycogenolysis and gluconeogenesis. b. Heredity. It is strongly associated with Type i" OM. c. Obesity. Adipose tissues are resistant to insulin. Therefore, glucose uptake by the cells is poor. d. Viral infections. Increase risk to autoimmune disorders that may affect the pancreas. e. Autoimmune disorders. Itis more associated with Type | DM. Thisis because it is the children who are more prone to viral infections that trigger autoimmune disorders. f. Waren. who are muttigravida with large babies. cae eee at in i pregnancy. us, hyperglycemia occurs during 602yalology of Diabotos Mttitus (om) INSULIN DEFICIENCY “yperalvoemia A. T blood osmolarity = ICF dehydration (b1 cells stv (blood attracts fluids from the cells; the B. Glycosuria * Glucose level exceed: for glucose is 180 = a threshold (renal threshold C. Polyuria = Glucose i i tubules 8S high osmotic pressure within the renal * Osmotic diuresis occurs * Hypovolemia = ECF dehydration D. Polydipsia = Results from ECF/ICF dehydration E. T blood viscosity = Sluggish circulation = Proliferation of eee Infections Periodontal (pyorthea) UTI Vasculitis Cellulitis Vaginitis (Candidiasis) Furuncles (single boils) : Carbuncles (boils that grow in groups) Retarded Wound Healing > Gangrene F. Polyphagia — the cells are starved & f Lipolysis (breakdown of fats) A. Hypertpidemia Atherosclerosis = Macroangiopathy - Brain: CVA - Heart: MI ‘ rene - Peripheral arteries: PVD's > 690 603v ty a. b. c. d. " Mf ay cataract — Blindness Neue Gord _> Autonomic Nervous System 0 Paralysis. (slow gastric emptying) © ae Bee ce ysincn + Peis ea ‘Acatone, Aceto — acetic acid, | blood pH - KETOACIDOSIS * Ketonuria & 7 Protein ee (-) Nitrogen balance A. TBUN, serum creatinine B. Tissue wasting C. Weight loss D. Debilitation pe | Diabetes Mellitus. . Also called Insulin Dependent Diabetes Mellitus (IDDM), juvenile - onset, brittle or unstable DM. Onset is before 30 years of age. Absolute deficiency of insulin is due to absence of Islet o Langerhans in the pancreas. The client is thin. This due to inability of the body to obtain gure from carbohydrates. al brotin for gl cia: the body breaks down fats - The client is prone to The ¢ diabetic ketoacidosis (DKA). In the absence fel, "a are metabotzed. ‘There ie inctoseed. prods The colt lborative a ketoacidosis, Hb lanagement for IDDM include: * Activity and : : ae exercise ays a component of management for IDDM). 604ype ll Diabetes Mellitus ‘ a ‘Aiso called Non — Insulin Dependent * maturity onset, ketosis — fesistant Diy ts Onset is after age 30 years, - With relative lack of insulin of Fesigt ; runeae " tance t usually insulin is sufficient to stabilize en°®.'© the action of insulin; not to deal with carbohydrate jet Protein t a ora Metabolism, Metabolism but , The client is prone to hyperglycem) * cama (HHNC). This is extreme rypeyt/PE3"Olr, non —kettc ay ‘ezutin dehytraton and vase realy without acidosis. It laborative manager incluc f. De 'gement for NIDDM include: « Activity and exercise * Oral Hypoglycemic Agents (OHA) o, \ Agents (HA) I hypoglycemia isunoonnoteae®,wPeaveemi * Insulin. In case of stress, surge: . infecti These conditions trigger stress . responses “md ches secretion of epinephrine, Norepinephrine and glucocorticoids. These hormones cause hyperglycemia. : Adeficiency in insulin results in hyperglycemia. The clinical manifestations of DM are as follows: a. ue Polydipsia, polyphagia (3 Ps) (more common in Type | ‘abetes Mellitus (NIDDM), AA b. Weight loss (more common in Type | DM). ¢. Blurred vision. 4d. Slow wound healing. e. Infections: pyorrhea (periodontal infections), urinary tract infection, vasculitis, cellulitis, furuncles, carbuncles, vaginal infections. Weakness and paresthesia. 9. Signs of inadequate circulation to the feet. h. Signs of accelerated atherosclerosis (renal, cerebral, cardiac, ’ Mi cpa ude artery disease, 'acrovascular complications _ incli coronary | a vaceamyopathy, hypertension, cerebrovascular disease, peripheral lar diseases and infection. ” Microvascular complications include retinopathy, nephropathy and y heutopathy, aed Diullaborative management for DM are as fol * Diet i. ce jally if client is obese. 50% i Ta calorie det, expociat ‘of 20% protein, 30% fats and Carbohydrates, deen 6057 jally vegetables. Fiber inhibits = High fiber diet, *Spestines and prevents hyperalycem gue absorption a be eaten, according to the dietary exchange na exchanges Mejent should not eat as MUCH fruits as he ait The cnn fructose that is converted into glucose Theta Fruits con much fruits may cause hyperglycemia. fore eating too carbohydrates like rice, bread, pasta, root crope . CO Simple carbohydrates like cakes, pastries are ha frely to cause hyperglycemia. fe ‘vil cise : b. denis Se ee ot regular pattern of exercise are as follows: o Exercise increases glucose uptake by the cells. Therefore, i lowers blood glucose levels. o Exercise lowers insulin requirements. o Exercise helps achieve desirable body weight. o Exercise helps maintain normal serum lipids. This reduces vascular risks. 7 «= Instruct client on dietary adjustments when exercising. * Instruct client to monitor blood glucose before, during and after the exercise period. = Initially, the client who requires insulin should be instructed to eat 15 g. carbohydrate snack {a fruit exchange or a snack of complex carbohydrate with a protein) before engaging in moderate exercise to prevent hypoglycemia = If blood glucose level is greater than 250 mg/dL and urinary ketones are present (DM Type 1), the client is instructed not to exercise until blood glucose is normal and urinary ketones are absent. c. Medications * Oral Hypoglycemic Agents e Stimulate Islet of Langerhans to secrete insulin, increas? Sensitivity of peripheral receptors to insulin, decrease hepatic glucose output or delay intestinal ab: ~ | sorption of glucose, decreasing serum glucose levels. 7 : - Indicated only in Type I! DM. 7 Drug interactions and Contraindications of OHA nd - Aspirin, al i » alcohol, —sulfonami ceptives monoamine oxida amides, — contracep! one aa iscreeee hypoglycemic off se inhibitors (MAOI's) incre’ yee fect, causi in blood 9l4 ‘ levels (hypogiy ia), using a decrease in rr J i 5 ycr@382 blood Mcoids, thiazide diuretics, and estrogen ino ‘ucose levels (hyperglycemia). 606. Sulfonylureas should prevent disulfiram. lke react Xe" With alcohol. To . Inderal (Propranolol) and other bets. d i may cane ypoatycemia, adrenergic blockers may cai i . Sulfonylureas, pny cause Gi gereytmias ‘ may occur. 'ypoglycemia > Sulfonylureas Dymelor (Acetohexamide) Diabenese (Chlorpropramide) Amaryl (Glimepiride) Glucotrol (Glipizide) Diabeta, Micronase (Glyburide) Tolinase (Ti ‘olazamide) Orinase (T. olbutamide) > Non — sulfonylureas Alpha Glucosidase Inhibitors Precose (Acarbose) Glyset (Miglitol) Biguanide Metformin (Glucophage) Meglitinide Starlix (Nateglinide) Prandin (Repaglinide) Thiozolidinediones Actos (Pioglitazone) Avandia (Rosiglitazone) en F WO Advise the client to wear a Medic — Alert bracelet. Insulin icated ir 1 DM ; ineicaes ee Il DM when diet and weight control are i i intail levels. raicte te oe mui can be admired intra ly in the emerge! ison ral anticoagulants, oral hypoglycemic Aspirin, Rocebimnern lockers, tricyclic oe i, tetracycline, and MAOT's increase the hypog! effects insulin, causing hyBOabeer otic, thyroid agents, oral barecacdereungr estrogen may cause 607nd stress can elevate blood lucos, pers ns, wle eu insulin. Insulin should not be wate Pica ard th n stress because hypergtycem; iam can ‘sult josiS ketoacid' of time of insulin is important because of The pea rane reactions occurring that OF the possibilty of MYON Te in are as follows: time. Th oa id acting or Rapid — acting Insulin Ha 45 mins. i ’ Ta (Lispro) %-thr. 2-4hrs. 5-7hrs. Wear Novolin R 3. Intermediate — acti ek Insulin NPH (Humulin 1 - 2 6-14hrs. 24 hrs. N; Novolin N) hrs. 4. Long — acting Insulin Besa” a SS a Ha (Humutin Uy hrs. 18-24 hrs. 24 hrs. 608Humulin 70/30 (70% ° NPH/30% Regular) tr) oa? AB 24 Lispro/Protamine75/25 10-15 F : 1-6 (75%Lispro mins. hrs. oe /25%Protamine) : Nursing Interventions in Insulin Therapy 4. The main route of insulin injection is subcutaneous. This promotes slower absorption and is less painful. There are lesser blood vessels and nerves in the subcutaneous areas. 2. The main areas for insulin injections are the abdomen, arms (posterior surface), thighs (anterior surface), and buttocks. 3. Administer insulin at 90°L. Most insulin syringes have needle gauge 27 to 29, that is about % inch long. 4. Do not massage injection site to prevent rapid absorption. Rapid absorption of insulin may cause hypoglycemia. 5. Injections should be % inch apart within the anatomical area. Finish all sites in one anatomical area before going to another area. ‘ 6. To prevent lipodystrophy (hard fatty masses in the subcutaneous layers): i Po a. Systematic rotation of the site of injection. Reuse one site after at least 2 to 3 weeks. ett b. Administer insulin at room temperature. Cold insulin causes | y- : : *Lipodystrophy inhibits insulin absorption. ial in between the paims to redistribute insulin i pales. eee shake the vial; bubbles make it difficult to aspirate ‘exact amount. 8. Storing Insulin: ; oud be kept in the - Prefilled Te syringe potent a 7 days (1 7 6097 uid be kept flat or with the neeq : syringes Son to prevent clogging of the need " an wef insulin will be used up in 30 days (1 Trot - ita via tat room temperature. Otherwise, ty ar Id be refrigerated. vial sr osing i in to extremes of temperat sing insulin to of ter ature, i Avoid rout nol be frozen or kept in direct suntight o, car. : ; 9. oe insulin may be mixed with any other type of insulin. F ; Sa tad i zinc suspensions (interm acting) may be ee ay wath each other and regular insulin; not with 1s of insulin. f 7 11 Se a raul. the following nursing actions are done: “a. Introduce air into the vial of intermediate — acting + iiatin (e.g. NPH). Do not aspirate / draw up the insulin, yet. : i f b. Introduce air into the vial of regular insulin, and draw up the insulin. Feet c. Draw up the intermediate — acting insulin (NPH). Remember: Draw up the regular insulin first. 12. Administer a mixed dose of insulin within 5 to 15 minutes of preparation; after this time the regular insulin binds with the NPH insulin and its action is reduced. 13.Monitor client for complications of insulin therapy: a. Local allergic reactions - Redness, swelling, tenderness and induration or wheal at the site of injection may occur 1 to 2 hours after administration. - Instruct the client to avoid the use of alcohol t0 cleanse the skin before injection. : ee one hour before injection S prescribed by ici: b. Insulin Lipedyatropsy ee ~ Lipoatrophy is loss of subcutaneous fat até ee as slight dimpling or more serious pitting Subcutaneous fat; the use of human insulin helps . 7 Prevent this complication. bohypertrophy is the development of fibrous hes} Teree at the injection site and is caused ‘ated use of an injection site. 610- Instruct the clie ys affe shee nt to avoid injecting insulin into - Instruct the client i insulin injection ates ‘he Importance of a - Instruct the client to temperature; not at cold c. Insulin Resistance - Li " ae be wee, Senstvty to the insulin from the - The client a 'yperalycemia. antibodies Gaining insulin develops immune decreasied th ‘at_bind with the insulin, thereby ant ani € insulin available for use in the body. Condition may be managed by administering a purer insulin preparation. d. Dawn Phenomenon - Results from the reduced tissue sensitivity to insulin that develops between 5:00 and 8:00 AM (prebreakfast hyperglycemia). This may be associated with nocturnal release of growth hormone. - Treatment is administering intermediate — acting insulin (NPH) at 10PM to control early morning hyperglycemia. e. Somogyi Phenomenon - Normal or elevated blood glucose levels are present at bedtime; hypoglycemia occurs at 2 to 3AM, which triggers production of counterregulatory hormones. - By 7AM, in response to the counterregulatory hormones, the blood glucose rebounds to hyperglycemic range (rebound hyperglycemia). - Treatment for Somogyi phenomenon _ includes decreasing the evening (predinner or bedtime) dose of intermediate — acting insulin, or increasing the bedtime snack. i lin Wanin. i ae progressive rise in the blood glucose level from ime to morning. ; : ce Tissier includes increasing the evening i i ediate — or it or bedtime) dose of intermedia 0 apa insulin before the evening meal if one is not already prescribed. inject insulin at room temperature. * Acute Complications of Diabetes Mellitus 61