Endocrine Anatomy and physiology

MEDSURG NURSING ENDOCRINE SYSTEM



ANATOMY AND PHYSIOLOGY  OVARY: Estrogen and Progesterone

 Hormones are natural chemicals that exert their effects on specific tissues known as  ADRENAL GLANDS

target tissues; which are located distant from and without any direct connection  Tent-shaped organs on the top of each kidney

with the endocrine gland.  ADRENAL CORTEX (outer portion)

 Endocrine glands are known as “ductless glands” and must use the blood to 1. Mineralocorticoids or Aldosterone (produced in the zona glomerulosa)-

transport secreted hormones to the target tissues. maintains extracellular fluid volume by prmoting sodium and water

 The endocrine system works with the nervous system to regulate overall body reabsoprtion and potassium excretion in the kidney tubules; secretion is

function and maintain homeostasis known as neuroendocrine regulation. regulated by the renin-angiotensin system, serum potassium ion

 Hormone-receptor actions work in a lock-and-key manner in that only the correct concentration, and ACTH

hormone can bind to and activate the receptor site. 2. Glucocorticoids or Cortisol (produced in the zona fasciculata and zona

 The control of cellular function by any hormone depends on a series of reactions reticularis)- affects carbohydrate(gluconeogenesis and perpiheral

working through negative feedback control mechanisms. glucose use), protein (protein catabolism), and fat (lipolysis)

 HYPOTHALAMUS metabolism, body’s response to stress (anti-inflammatory), emotional

 Located beneath the thalamus on each side of the third ventricle of the brain stability, and immune function (polymorphonuclear leukocytes); peaks

 Shares a closed circulatory system with the anterior pituitary gland known in the morning and reaches its lowest level 12 hours after each peak

as the hypothalamic-hypophysial portal system, which allows hormones 3. Androgens and Estrogens (produced in the zona fasciculata and zona

produced in the hypothalamus to travel directly to the anterior pituitary reticularis)

gland  ADRENAL MEDULLA (inner portion)

 Nerve fibers in the hypophysial stalk connect the hypothalamus to the 1. Catecholamines (Epinephrine and Norepinephrine)- not essential for life

posterior pituitary gland but play a role in the physiologic stress response (fight or flight)

 FUNCTION: To produce regulatory hormones (releasing hormones)  THYROID GLAND

 PITUITARY GLAND  Located in the anterior neck and directly below the cricoids cartilage

 Located at the base of the brain in the valley of the sphenoid known as the 1. Thyroxine (T4) and Triiodothyronine (T3-most active form) (produced by

sella turcica the follicular cells)- increase metabolism (BMR) which causes an increase

 ANTERIOR LOBE (ADENOHYPOPHYSIS) in oxygen use and heat production in all tissues; release is stimulated by

1. Thyroid-stimulating hormone (TSH)- stimulates synthesis and release of cold and stress; act as insulin antagonist

thyroid hormone 2. Thyrocalcitonin (TCT) (produced by the parafollicular cells)- lowers serum

2. Adrenocorticotropic hormone (ACTH)- stimulates synthesis and release of calcium and serum phosphorous levels by reducing bone resorption or

corticosteroids and adrenocortical growth breakdown

3. Luteinizing hormone (LH)- stimulates ovulation, progesterone, and  PARATHYROID GLAND

testosterone secretion  Consist of four small glands located close to, embedded in, or attached to the

4. Follicle-stimulating hormone (FSH)- stimulates estrogen secretion, follicle back surface of the thyroid gland

maturation, and spermatogenesis 1. Parathyroid hormone (PTH)- regulates calcium and phosphorous

5. Prolactin (PRL)- stimulates breast milk production metabolism by acting on bone (bone resoprtion) , kidney (activates

6. Somatotropin or Growth hormone (GH)- promotes growth through vitamin D and calcium reabsorbtion), and the intestinal tract

lypolysis, protein anabolism, and insulin antagonism  PANCREAS

7. Melanocyte-stimulating hormone (MSH)- promotes pigmentation  Lies behind the stomach and has endocrine (islets of Langerhans) and

 POSTERIOR LOBE (NEUROHYPOPHYSIS) exocrine functions

1. Vasopressin or Antidiuretic hormone (ADH)- promotes water 1. Glucagon (alpha cells)- increases blood glucose levels by causing

reabsorption glycogenolysis, gluconeogenesis, lipolysis, and ketone formation

2. Oxytocin- stimulates uterine contractions and ejection of milk 2. Insulin (beta cells)- promotes movement and storage of carbohydrate,

 GONADS protein, and fat therefore lowering blood glucose levels

 Male (testes) and female (ovaries) reproductive endocrine glands 3. Somatostatin (delta cells)- inhibits release of glucagon, insulin, and GI

 Although these glands are present at birth, their function does not begin peptides

until puberty

 TESTES: Testosterone



ENDOCRINE DIRSORDERS

DISORDERS MANIFESTATIONS MANAGEMENT

Hypopituitarism Gonadotropin  Testicular failure: testosterone and Neurologic Assessment:

sterility  Peripheral vision: diplopia (double vision)

*Sheehan’s Syndrome: post-  Ovarian failure: amenorrhea, dyspareunia  Temporal headaches

partum hemorrhage and infertility  Muscular paralysis

hypotensionischemia GH (Dwarfism)  somatomedins  Limiting eye movement

pituitary infarction (necrosis)  decreased bone density (osteoporosis)  Hypometabolism

 pathologic fractures  Hemianopsia

*Simmond’s Disease or  muscle strength Laboratory Findings:

Panhypopituitarism (total absence  serum cholesterol levels  Stimulation tests (injecting agents that are known to stimulate secretion of

of all pituitary secretions) TSH (Secondary  circulating thyroid hormone levels specific pituitary hormones and then measuring the response)

Hypopituitarism)  weight gain insulinGH or ACTH

*Primary Hypopituitarism  cold intolerance TRHTSH

(problems arising within the  scalp alopecia GnRHLH and FSH

anterior pituitary itself)  hirsutism Diagnostics:

 menstrual abnormalities  Skull x-rays

*Secondary Hypopituitarism  libido  CT scan

(problems in the hypothalamus  slowed cognition  MRI

that change anterior pituitary  lethargy  Angiogram

function) ACTH (Addison’s  serum cholestrerol Interventions:

Disorder)  pale, sallow complexion  Androgen therapy (SE: gynecomastia, acne, baldness, prostate enlargement)

 malaise and lethargy  Estrogen and Progesterone therapy (SE: hypertension, thrombosis)

 anorexia  Clomiphene citrate (to induce ovulation)

 postural hypotension  GH injections

 headache  Surgical removal of tumor

 hypoglycemia  Radiation

 hyponateremia

 axillary and pubic hair (women)

Hyperpituitarism PRL  galactorrhea Assessment:

 amenorrhea  Change on hat, shoe, ring, or glove size

*most common cause: pituitary  infertility  Fatigue or lethargy

adenoma GH (Gigantism or  Gigantism (before puberty): rapid  Backache and athralgia

Acromegaly) proportional growth in the length of the  Headaches

bones  Changes on vision

 Acromegaly (after puberty): increased  Menstrual changes

skeletal thickness, hypertrophy of the skin,  Decreased libido

enlargement of visceral organs (liver and  Dyspareunia

heart)  Difficulty in chewing and dentures that no longer fit

 hyperglycemia  Arthritic changes causing joint pain and mobility

 in lip and nose sizes, and a prominent  Fingers and toes with arrow-head shape at tips

brow ridge, and head, hand and foot sizes  Metabolism and strength

 prognathism (projection of the jaw beyond  Lethargy and weakness

the facial features)  Perspiration and oil secretion in the skin

 organomegaly Laboratory Findings:

 hypertension  Hormone elevation

 dysphagia (enlarged tongue) Diagnostics:

 deepening of the voice (hypertrophy of  Skull x-rays

larynx)  CT scan

 MRI

 Angiogram

 Suppression test (giving the agents that induce a suppressed response from

the pituitary gland, and they can determine whether the normal feedback

control mechanisms for hormonal regulation are intact)

Interventions:

 Encourage the client to express concerns and fears about his or her altered

physical appearance

 Drug Therapy:

- Dopamine agonists: bromcriptine mesylate (Parlodel), cabergoline

(Dostinex) SE: orthostatic hypotension, gastric irritation, nausea,

headache, abdominal cramps, constipation

- Somatostatin analogues: octreotide (Sandostatin)

- GH receptor blocker: pegvisomant (Somavert) SE: gallbladder disease

and tumor size

 Radiation

 Surgery: Transsphenoidal Hypophysectomy (incision above the upper lip

and reaches the pituitary gland through the sphenoid sinus)

- nasal and oral mucous membrane swab specimens for bacterial C&S

before surgery because the surgery can move microorganisms from

these areas into the blood and cause systemic infection

- monitor neurologic response and document changes in vision, mental

status, altered LOC, or strength of extremities

- observe for transient diabetes insipidus (monitor I&O, urine specific

gravity, vasopressin as indicated, F/C and daily weight)

- teach client to report postnasal drip (check if CSF through Halo sign or

glucose test)

- teach the client to avoid coughing early after surgery because it ICP

and may lead to CSF leak

- deep breathing exercises to prevent pulmonary problems

- frequent mouth rinses, dental floss, and apply petroleum jelly to dry

lips

- assess for meningitis (fever, headache, nuchal rigidity)

- antibiotics, analgesics, antipyretics as ordered

- monitor neurological status q1 for the first 24 hours then q4

- instruct client to avoid bending at the waist because it ICP

- monitor nasal drip pad for type and amount of drainage

- monitor bowel movements to prevent constipation and straining

- teach self-administration of hormones

Diabetes Insipidus (ADH)  polyuria Assessment:

 dehydration  Measure 24 hour fluid I&O

*distal kidney tubules and collecting ducts remain  urine SG  Do not restrict food and fluids

impermeable to water  plasma osmolarity  UO 4-30L/day

 polydipsia  Urine SG 5mg/dL (normal value) needs further testing

 3-Day Low Dose Dexamethasone Suppression Test: instruct client not to

take drugs for at least 2 days before the test and no stressful procedures

(barium enema, myelogram, intense physical therapy); day1: baseline 24-

hour urine sample; days 2&3: dexamethasone 0.5mg q6 then 24 hour urine

testing; if cortisol levels needs further testing (normal: urinary 17-

hydroxycorticosteroid excretion and cortisol levels suppressed by

dexamethasone)

 High-Dose Dexamethasoe Suppression Test (distinguishes between bilateral

adrenocortical hyperplasia and adrenocortical neoplasm): overnight or 2-day

test injection of 8mg dexamethasone; if plasma cortisol that is 50% less

than baselineCushing’s disease

Interventions:

 Weigh client daily and monitor I&O to assess hydration status

 Fluid restriction as indicated

 Drug Therapy:

- Mitotane (Lysodren): adrenal cytotoxic agent used for inoperable

tumors

- Aminogluthethimide (Epliten, Cytadren)

- Metyrapone (Metopirone)

- Cyproheptadine (Periactin): interferes with ACTH production

 Radiation (assess for neurologic status, headache. BP or PR,

disorientation, changes in pupillari size or reaction, skin dryness, redness,

flushing, or alopecia)

 Surgery:

- Removal of pituitary adenoma

- Total hypophysectomy

- Adrenalectomy

 Correct electrolyte imbalances before surgery (sodium, potassium, chloride)

 Carding monitoring for dysrhythmias

 Control hyperglycemia before surgery

 Prevent infection with handwashing and aseptic technique

 Decrease risk of falls by raising side rails and encouraging client to ask for

assistance when getting out of bed

 High calorie and high protein diet before surgery

 Glucocorticoids before and during surgery to prevent adrenal crisis

 CCU: assess client q15minutes for shock (BP, rapid and weak pulse, UO)

 Monitor VS, hemodynamic variables, I&O, daily weight, and serum

electrolytes post-op

 Lifelong glucocorticoid replacement after bilateral adrenalectomy

 Assess skin for reddened areas, excoriation, breakdown, and edema

 If mobility decreased, turn client q2 and pad bony prominences

 Avoid activities that may result to skin trauma

 Use soft toothbrush and electric shaver

 Keep skin clean and dry after washing

 Moisturizing lotion for excessive skin dryness

 Use tape sparingly and use caution when removing

 Exert pressure over site of puncture longer than normal to prevent bleeding

and bruising

 When moving client in bed, use lift sheet instead of grasping

 Ambulatory aids

 High calorie, calcium, and vitamin D diet

 Avoid caffeine and alcohol which promote GI ulcers and bone density loss

 Antacids and H2-blockers on regular schedule

 Avoid aspirin

Hyperaldosteronism  hypernatremia (BP and suppress renin Diagnostics:

production)  Laboratory studies

*Primary Hyperaldosteronism or Conn’s Syndrome  hypokalemia  X-rays

(results from excessive secretion of aldosterone from one  metabolic alkalosis  CT scan

or both of the adrenal glands caused by adrenal  rare peripheral edema due to “renal escape  MRI

adenoma) mechanism” (kidney decrease sodium  plasma renin

reabsorption)  potassium, sodium

*Secondary Hyperaldosteronism (high levels of  headache  aldosterone

angiotensinII that are stimulated by high plasma levels of  fatigue  H+ loss, blood pH

renin caused by renal hypoxemia or thiazide diuretics)  muscle weakness  USG

 nocturia Interventions:

 polydispsia  Surgery: Adrenalectomy

 polyuria  Drug Therapy:

 paresthsias - Spirinolactone: potassium diuretic (avoid potassium supplements and

 visual changes rich foods and increase dietary sodium) SE: hyponatremia, dryness of

the mouth, thirst, lethargy, drowsiness

- Potassium supplements

 Low sodium diet before surgery

 Glucocortcoid replacement

Pheochromocytoma  intermittent episodes of hypertension or Diagnostics:

attacks  24 hour urine collection for Vanillylmandelic acid (VMA-product of

*catecholamine producing and storing tumor that arises *tricyclic antidepressants, droperidol, cathecholamine metabolism), metanephrine, and cathecholamine

in chromaffin cells glucagon, metoclopramide, *restrict caffeine, citrus fruits, bananas, vanilla-containing foods, licorice,

phenothiazenes, naloxaone, tyramine rich aspirin, and antihypertensive drugs

*epinephrine and norepinephrinealpha and beta foods can induce hypertensive crisis  Plasma cathecholamines are elevated after the client has rested for 30

receptor activitymimic SNS effects  severe headaches minutes

 palpitations  Clonidine Suppression Test: for inconsistent results; cathecholamines

*hallmark: HPN  profuse disphoresis remain elevated

 flushing  Cathecholamine Stimulation Test

 apprehension  MRI

 sense of impending doom  CTscan

 chest or abdominal pain Interventions:

 nausea and vomiting  Surgery: Adrenalectomy

 IAP  Monitor BP regularly and place cuff consistently on the same arms with the

 urinary frequency client in standing and lying positions

 heat intolerance  Identify and avoid stressors

 weight loss  Do not smoke, drink caffeine, or change positions suddenly

 tremors  DO NOT PALPATE ABDOMEN: sudden release of cathecholamines and sever

hypertension

 Calorie, vitamin, and mineral rich diet

 Maintain hydration status

 Calm, resting environment for client with severe headache

 Limit activity

 Provide darkened, private room to promote rest (avoid interruptions)

 Drug Therapy:

- alpha-adrenergic blockers for HPN, tachycardia, and dysrhythmias:

Phenooxybenzamine (Dibenzyline), Propranolol (Inderal, Detensol),

Labetalol (Trandate)

- calcium channel blockers: Nicardipine (Cardene)

- agents to cathecholamine synthesis: Metyrosine (Demser)

 Avoid beta-adrenergic blockers to prevent rebound HPN

 Closely monitor for hypotension and hypovolemia post-op (hemorrhage and

shock)

 Monitor VS, I&O

Hyperthyroidism  unusual diaphoresis (wears lighter clothing Assessment:

in cold weather)  Record age, gender, and usual appetite

*the manifestations of hyperthyroidism are called  palpitations or chest pain  Client may report weight loss, increased appetite, and increased number of

thyrotoxicosis  dyspnea with or without exertion bowel movements per day

 earliest problem the client notices: visual  Change in energy level or in the ability to perform ADLs

*causes hypermetabolism and SNS activity changes due to opthalmopathy (abnormal  Past thyroid surgery or neck radiation therapy

*protein degradation > protein synthesisnegative eye appearance or function)  Ask present antithyroid drugs of thyroid hormones

nitrogen balance -eyelid retraction (eyelid lag): occurs in  Ask client to look up and down and document responses

*glucose tolerancehyperglycemia all forms of thyrotoxicosis, the upper eyelid Laboratory Findings: T3, T4, T3 resin uptake, TSH, TSH-antibodies

*fat metabolismbody fat fails to descend when the client gazes Diagnostics:

*increased appetite but energy demand > food slowly downward  Thyroid scan: evaluates the position, size, and functioning of the thyroid by

intakeweight losschronic nutritional deficiency -globe lag (eyeball lag): upper eyelid giving radioactive iodine per orem and measuring RAIU *discontinue iodine

pulls back faster when the client gazes containing drugs 1 week before and procedures using iodine containing dye

*NOT ALL CLIENTS WITH GOITER HAVE upward 4 weeks before the scan

HYPERTHYROIDISM  fatigue  Ultrasonography: determine size and composition of masses and nodules

 weakness  ECG

*CAUSES:  insomnia Interventions:

-Grave’s Disease (toxic diffuse goiter):  changes in menses: amenorrhea or  Monitor apical pulse, BP, temperature at least q4

autoimmune disorder in which antibodies (TSIs) are made menstrual flow  Instruct client to report palpitations, dyspnea, vertigo, or chest pain

and attach to TSH receptor sites causing the thyroid  libido immediately

gland to increase in size and overproduce thyroid  exopthalmos (wide-eyed or startled look):  Encourage rest

hormones (hyperthyroidism, exopthalmos, pretibial due to edema in the extraocular muscles  Keep environment quiet as possible

myxedema) and fatty tissue behind the eye which  Frequent bed line changes, sponge baths, and cool environment

-Toxic Mulitnodular Goiter: hyperthyroidism pushes the eyeball forward and pressure  Drug Therapy:

caused by multiple thyroid nodules; absence of on the optic nerve - Antithyroid drug (block thyroid hormone production): thioamides,

exopthalmos and pretibial myxedema  corneal ulcers or infection PTU, methimazole (Tapazole), and carbimazole (Neo-Mercazole)

-Exogenous Hyperthyroidism: hyperthyroidism  excessive tearing and bloodshot - Iodine (thyroid size, vascularity and blood flow to the thyroid

caused by excessive use of thyroid replacement hormones appearance which reduces hormone production and release)

 photophobia - Lithium carbonate (inhibits thyroid hormone release) SE:

*thyroid storm or crisis is a life-threatening condition  bruits (turbulence from increased blood depression, DI, tremors, N/V

that can occur when hyperthyroidism is left untreated or flow) - Beta blockers (Propranolol):relieve diaphoresis, anxiety,

poorly controlled or when the client is severely stressed  systolic BP tachycardia, palpitations

 tachycardia  Radioactive Iodine Therapy (not used in pregnant women because it crosses

*hallmark: heat intolerance  dysrhythmias the placenta and can damage the fetal thyroid gland)

 diastolic BP  Surgery: Total/Subtotal Thyroidectomy (collar incision with parathyroid left

*GOITER CLASSIFICATION:  widened pulse pressure behind)lifetime thyroid hormone replacement (total)

0-no palpable or visible goiter  fine, soft, silky hair and smooth, moist skin  Return client to euthyroid before surgery

1-mass not visible with head in normal position but  muscle weakness  High-protein and high –carbohydrate diet

palpated and moves up when swallowing  hyperactive DTR  Coughing and deep breathing exercises (support neck when coughing and

2-massvisually asymmetric and easily palpated  tremors moving with both hands behind neck to reduce tension on suture line)

 restless and irritable  Explain hoarseness of voice post-op

 mood swings and attention span  Monitor VS q15minutes post-op until stable and then q30minutes

 Use sandbags or pillows to support head and neck

 Semi-Fowler’s position

 Avoid neck extension

 Analgesics as needed

 Elevate HOB at night and use artificial tears

 Dark glasses or eye patches for photophobia

 Tape lids with non-allergic tape

 Prednisone, diuretics, or orbital decompression for infiltrative

opthalmopathy

Complications:

 Hemorrhage: during first 24 hours after surgery; inspect neck dressing and

behind the client’s neck for blood

 Respiratory Distress: stridor is heard in acute respiratory obstruction; keep

emergency tracheostomy, oxygen, suction at bedside

 Hypocalcemia and Tetany: due to PTH; assess for tingling around mouth,

toes, fingers and muscle twitching; ready calcium gluconate or calcium

chloride per IV at bedside

 Laryngeal Nerve Damage: temporary hoarseness and weak voice; assess

voice at 2-hour interval and document changes

 Thyroid Storm: triggered by stressors (trauma, infection, diabetic

ketoacidosis, pregnancy), exposure to iodine, vigorous palpation of the

goiter, RAI; KEY MANIFESTATIONS: fever, tachycardia, systolic HPN, GI

distress, restlessness; INTERVENTIONS: maintain airway, give antithyroid

drug, propranolol, sodium iodide solution glucocorticoids, and

antipyretics as prescribed, monitor VS q30minutes, PNSS, cooling blanket

and ice packs





Hypothyroidism  time spent sleeping (14-16 hours) Laboratory Findings: T3, T4; primary:TSH; secondary:TSH

 generalized weakness Interventions:

*dysfunctional thyroid or insufficient iodine or  anorexia  Respiratory Monitoring:

tyrosineTHmetabolic rateTSH by hypothalamus  muscle aches - Monitor rate, rhythm, depth, and effort of respirations

and anterior pituitary gland TSH binds to thyroid  paresthesias - Note chest movement, symmetry, and retractions

cellsgoiter  constipation - Check for bradypnea, dyspnea and paradoxical motion

 cold intolerance (more blankets at night or - Note changes in SaO2 and ABG

*cellular energy and metabolites build up inside cells sweater and extra clothing in warm - Monitor client’s ability to cough effectively

(glycoaminoglycans)mucous and water weather)  Shock Prevention: BP, UO, change in mental status

(myxedema)non-pitting cellular edema (around the  libido - Monitor temperature and respiratory status

eyes, hands and feet, between shoulder blades, tongue  difficulty in becoming pregnant and - Monitor BP, skin color, heart sounds and rhythm, peripheral

and larynx)change in organ texture changes in menses (heavy, prolonged pulses, and capillary refill

bleeding or amenorrhea) - Monitor signs of inadequate tissue oxygenation (restlessness and

*myxedema coma is a rare, serious complication of  impotence and infertility apprehension)

untreated or poorly treated hypothyroidism which causes  edema around the eyes and face - Monitor I&O

heart muscles to be flabby and chamber size to  blank expression - Administer oxygen or mechvent as needed

increaseCO and perfusion to the brain and other  thick tongue - Administer antiarryhthmic agents as ordered

vital organsorgan failure  slow muscle movement  Hypothermia Treatment:

 most common reason for seeking medical - Monitor temperature and VS, and skin color

*most common cause: RAI attention: depression - Place cardiac monitor as appropriate

 lethargy, apathy, drowsy, withdrawn - Cover with warm blankets and adequate clothing

*CAUSES: thyroidectomy, radiation, autoimmune thyroid  impaired memory and attention span - Administer heated oxygen

destruction, thryroid cancer, iodine deficiency, excessive - Avoid giving IM or SQ medications during hypothermia

exposure to iodine, lithium, phenylbutazone, PTU, - Give client warm oral fluids and consume adequate caloric intake

sodium or potassium perchlorate, aminiglutethimide,  Lifelong thyroid hormone replacement (lowest dose and gradual increase to

thiocyanates, cobalt prevent HPN. heart failure, and MI)

 Instruct client to report episodes of chest pain or discomfort immediately

*hallmark: cold intolerance  Orient client and assess mental status

 Provide safe environment

Acute Thyroiditis (bacterial invasionneck tenderness,  Emergency Care for Myxedema Coma:

fever, dysphagia) - Maintain patent airway

- Replace fluids with IV normal or hypertonic saline

Subacute or Granulomatous Thyroiditis (viral - Give levothyroxine sodium, glucose IV, corticosteroids as prescribed

infectionfever, dysphagia, joint pain) - Check temperature q1

- Cover with warm blankets

Chronic Thyroiditis or Hashimoto’s Disease - Monitor changes in mental status

(autoimmune disorder which destroys thyroid tissue) - Turn q2

- Institute aspiration precautions

Thyroid Cancer (papillary, follicular, medullary,  Adequate fluid and fiber to prevent constipation

anaplastic)  Adequate rest

 Encourage family to voice out concerns



Hyperparathyroidism  waxy pallor of the skin Assessment:

 bone deformities in the extremities and  Ask about bone fractures, recent weight loss, arthritis, or psychological

*PTHkidney reabsorption of calcium and phosphate back distress

excretionhypercalcemia and hypophosphatemia  renal calculi and calcium deposits at soft  Past neck or head radiation

*PTHosteoblast and osteoclastbone resoprtion or tissues of the kidney Laboratory Findings: serum PTH, calcium and phosphate levels, urine cAMP

bone losscalcium deposited in soft tissues  bone lesions (pathologic fractures, bone Diagnostics:

cysts, osteoporosis)  x-ray (kidney stones and bone lesions)

*most common cause: beneign tumor in parathyroid  anorexia  Arteriography

(hypocalcemia and vitamin D deficiency)  nausea and vomiting  CT scan

 epigastric pain  Venous catheterization of thyroid veins

 constipation  Ultrasonography

 weight loss Interventions:

 serum gastrinpeptic ulcer disease  Hydration (IV saline) and furosemide (Lasix): a diuretic which calcium

 fatigue and lethargy excretion

 psychosis and mental confusion  Monitor cardiac function and I&O q2-4

(>12mg/dL)  Report precipitous drop of serum calcium which may cause tingling and

 damage of laryngeal nerve may cause voice numbness

hoarseness  Drug Therapy:

- Oral phosphates (inhibit bone resoprtion and interfere with calcium

absorption)

- Calcitonin and glucocorticoids (release of skeletal calcium and

excretion of calcium)

- Calcium chelators: Mithramycin (SE: thrombocytopenia and kidney

liver toxicity; monitor liver function) and Penicillamine (Cuprimine,

Pendramine)

 Surgery: Parathyroidectomy

 Stabilize calcium levels before surgery

 Coughing and deep breathing exercises

 Talking may be painful 2 days post-op

 Neck support by placing both ahnds behind the neck to assist in elevating

the head

 Observe for respiratory distress which may occur from compression of

trachea by hemorrhage or neck swelling

 Keep suction, oxygen, and tracheostomy at bedside

 Monitor VS and bleeding

 Check for hypocalcemic crisis (Trousseau’s and Chvostek’s signs)

 Lifelong treatment of calcium and vitamin D post-op

Hypoparathyroidism  tingling and numbness around the mouth Assessment:

or in the hands and feet  Ask about mild tingling and numbness

*Iatrogenic Hypoparathyroidism (due to total  severe muscle cramps  Past neck or head radiation

parathyroidectomy)  carpopedal spasms Laboratory Findings: serum PTH, calcium and phosphate levels, urine cAMP

*Idiopathic Hypoparathyroidism (due to unknown cause  seizures (without loss of consciousness or Diagnostics:

or autoimmune) incontinence)  X-ray (kidney stones and bone lesions)

 irritability or psychosis  Arteriography

*hypomagnesemia (alcoholic or malabsoprtion) interfere  bands or pits may encircle the crowns of  CT scan

with PTH effect on kidneys and bones the teeth (loss of calcium and enamel loss)  ECG

 Blood test

Interventions:

 IV calcium as 10% solution of calcium chloride or calcium gluconate over

10-15 minutes

 Calcitrol (Rocaltrol) 0.5-2mg daily for acute vitamin D deficiency

 50% magnesium sulfate 2mL doses per IM or IV to correct hypomagnesemia

 Calcium intake 0.5-2g daily

 50,000-400,000 units ergocalciferol daily for long tern therapy

 Instruct to eat foods high in calcium but low in phosphorous (avoid milk,

yogurt, and processed chees)

 Stress lifelong therapy for hypocalcemia to prevent hypocalcemic crisis

Diabetes Mellitus (Chronic Hypergycemia)  Polyuria (osmotic dieresis caused by excess Laboratory Findings:

glucose in the urinesodium, potassium,  Blood glucose values

*Type1 (insulin deficiency): autoimmune disorder in chloride, water)  Fasting Blood Glucose Test (do not eat any food or drink any liquid for at

which beta cells are destroyed in a genetically susceptible  Polydipsia (due to dehydration) least 8 hours; water is permitted)

person  Polyphagia (because cells receive no  Oral Glucose Tolerance Test (most sensitive test for diagnosing DM;

*Type2 (insulin resistance): progressive disorder in which glucosecell starvation) carbohydrate restrictions or bed rest alters results; client drinks a beverage

the pancreas makes less insulin over time)  ketone bodiesmetabolic acidosis containing glucose load of 75g and blood samples are collected at 30

*GDM (pregnancy)  dehydrationhemoconcentration, minute intervals for 2 hours; DM=200mg/dL at 120 minutes)

hypovolemia, hypoperfusion,  Glycosylated Hgb Assays (shows the average blood glucose level during the

*METABOLIC SYNDROME (SYNDROME X): group of hypoxiablock Kreb’s cyclelactic acid previous 120 days)

disorders with insulin resistance or obesity as a main  H+ and CO2Kussmaul respiration  Glycosylated Serum Proteins and Albumin (viable for 14 days)

feature  fruity (acetone) breath or odor  Urine Testing for Ketones

 Macrovascular Complications:  Urine Testing for Renal Function

*liver is the first organ to be reached by insulin in the - Coronary heart disease (most common  Urine Testing for Glucose

bloodglycogenesis, gluconeogenesis, glycogenolysis, complication of DM; MI is the leading  ICAs

ketogenesis cause of death in clients with DM)  C-peptide levels

- Cerebrovascular disease ( Interventions:

*basal insulin secretion (low levels during fasting) - Peripheral vascular disease  Drug Therapy

*prandial insulin secretion (high levels during eating)  Microvascular Complications: - Oral: sulfonylurea, meglitinide, biguanide, alpha-glucosidase,,

- Nephropathy (DM is the leading cause thiazolidenidione, combination agents) *antidiabetic drug is not a

*blood glucoseglucagon glycogenesis, of ESRD; microalbunimemai is the substitute for dietary modification and exercise

gluconeogenesis (lipolysis and proteolysis) and earliest sign - Insulin Therapy (1.abdomen[2 inch radius from the navel] 2. deltoid

glycogenolysis - Neuropathy(excess 3. thigh 4. buttocks) *rotate sites to prvent lipohypertrophy or

glucosesorbitolimpaired motor lipoatrophy

*THREE THEORIES FOR DIABETIC VASCULAR function; constipation is the most  Diet and Exercise

COMPLICATIONS: common GI symptom, gastroparesis is  Surgery: Pancreas Transplantation

1. chronic hyperglycemia causes irreversible structural a cause of hypoglycemia)  Wound and Foot Care: foot injury is the most common complication of Dm

changes resulting in basement membrane thickening and - Retinopathy (NPDR, PDR or leading to hospitalization

organ damage neovascularization, microaneurysms,  HYPOGLYCEMIA

2. glucose toxicity directly or indirectly affect functional venous beading) Causes:

cell integrity - Omission of meals

3. chronic ischemia in microcirculatory branches causes - Overdose of Insulin

connective tissue hypoxia and microischemia - Strenuous exercise

- GI upset

*Dawn Phenomenon: night time release of GH that Assessment

causes blood glucose elevations at about 5-6AM (treated - Restlessness

by providing more insulin for the overnight period) - Hunger pangs

*Somagyi’s Phenomenon: morning hyperglycemia from - Yawning

the effective counter-regulatory response to night time - Weakness

hypoglycemia (treated by ensuring adequate dietary - Tremors

intake at bedtime and evaluating insulin dose and - Pallor

exercise program) - Diaphoresis

- Cold, clammy skin

- Headache

- Dizziness

- Faintness

- Tachycardia

- Abdominal pain

- Blurred vision

- Slurred speech

- Urine (-) CHO

- Altered LOC

Management:

- Simple sugars per orem

o 3-4 oz. regular softdrink

o 8oz. fruit juice

o 5-7 pcs. Lifesaver’s candies

o 3-4 pcs. hard candies

o 1 tbsp. sugar

o 5 ml. pure honey / Karo syrup

o 10-15 gms. CHO

- D50 W 20-50 ml/IV push

- Monitor blood sugar

- Patient teaching

 DIABETIC KETOACIDOSIS (sudden): insulingluconeogenesis and

glycogenolysislipolysis and proteolysisketone formation and

BUNhyperglycemiaosmotic diuresisdehydration and acidosis

- First assess airway, LOC< hydration status, electrolytes and glucose level

- Closely assess client’s fluid status (IVF PNSS and D5 0.45%

- Watch for signs of hypokalemia, including fatigue, malisise, confusion,

muscle weakness, shallow respirations, abdominal distention or paralytic

ileus, hypotension, and weak pulse

- Before giving IV potassium, make sure that the client produces at least

30mL/hour urine

- Bicarbonate for severe acidosis

 HYPERGLYCEMICHYPEROSMOLAR NONKETOTIC SYNDROME AND COMA

(gradual): insulingluconeogenesis and

glycogenolysishyperglycemiaosmotic diuresisextracellualr

dehydrationrenal insufficiency and hypokalemiashocktissue

hypoxiacoma

- Rehydrate and restore normal glucose level within 36-72 hours\assess q1

for signs of cerebral edema; abrupt changes in mental status, abnormal

neurologic signs, and coma

- Immediately report changes in LOC, changes in papillary size, shape,

reaction, or seizure

- IV isulin at 10units/hour