endo alterations

7/31/2019 Endo Alterations

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PITUITARY GLANDHYPOPITUITARISM decreased secretion of one or more of the

eight hormones produced by the pituitarygland

Panhypopituitarism most hormones

ETIOLOGIC CAUSES:

disease of the pituitary gland itself disease of the hypothalamus can result from radiation therapy (head

and neck area) total destruction from trauma,

tumor/vascular lesion which removesall stimuli

DWARFISM

GENERALIZEDLIMITEDGROWTH

CATEGORIES:

Disproportionate

small body but other parts are ofaverage size or above average size

example: Dagul

Proportionate everything is proportionate but

small in nature

example: Mahal and Mura

TYPES:

Genetic or Mid-parental height

boys height: (+ 5in to mothersheight) + fathers height = total / 2

girls height: ( - 5in from fathersheight) + mothers height = total /2

Constitutional Stature

short in nature Psychosocial Dwarfism

due to an emotional problem Catch-up Growth

present during puberty stage

CLINICAL MANIFESTATIONS:

approximately 4ft in height average size trunk short arms and legs short fingers limited mobility progressive development of bowed

legs progressive development of swayed

lower back (Kyphotic)

NURSING INTERVENTION:

provide emotional support to thefamily

encourage client and family to expressfeelings

administer prescribed GH

DIABETES INSIPIDUS

HYPOSECRETIONOFADH

DISORDER OF WATER METABOLISM CAUSED BY

DEFICIENCYOFADHSECRETEDBYPPGORINABILITYOF

THEKIDNEYTORESPONDTOADH (NEPHROGENICDI)

DEFICIENCYADHMAYBEPARTIAL/COMPLETE

DIMAYBEPERMANENT/ TRANSIENT

ETIOLOGIC FACTORS:

Primary

idiopathic

Secondary

head trauma, neurosurgery (braintumor), aneurysms, conditions that

ICP, surgical removal of posterior

pituitary tumor, CNS infections Nephrotic Diabetes Insipidus

failure of renal tubules to respondto ADH

longstanding renal disease (r/hypokalemia, hypercalcemia) andother meds

DIAGNOSTIC TESTS:

Fluid deprivation test

withholding fluid for 8-12hours/until 3-5% body weight is lost

Plasma and urine osmolality studie

inability to SG and osmolality =DI

Na level Plasma levels, desmopressin (synthetic

vasopressin), IV infusion (hypertonic)

CLINICAL MANIFESTATION:

marked polyuria (4L/day)

USG: 1.001 - 1.005 polydipsia (2-20L), craves cold water dehydration muscle pain and weakness postural hypotension and tachycardia urine is like water

MEDICAL MANAGEMENT:

GOALS: replace ADH, adequate fluidreplacement, correct underlying

intracranial pathology Desmopressin

without vascular effects of naturaADH = fewer adverse effects

administered intranasally viacalibrated plastic tube

Vasopressin causesvasoconstriction; used cautiouslywith CAD

IM administration of ADH

if intranasal route is not possible

done every 24 96 hours

vial of med should be shaken

rotation of injection to prevent

lipodystrophy Clofibrate (Atromid-S)

hypolipidemic agent withantidiuretic effect on px with DI

Chlorpropamide (Diabinese) andthiazide diuretics

used in mild forms as it potentiatethe actions of Vasopressin

Tx for nephrogenic DI

thiazide diuretics

mild salt depletion

prostaglandin inhibitors andindomethacin


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NURSING MANAGEMENT:

demonstrate correct medadministration

provide s/sx of hyponatremia instruct px to wear medical bracelet

HYPERPITUITARISM ETIOLOGIC CAUSES:

Sheehans syndrome

Postpartum pituitary necrosis

severe blood loss, hypovolemia,HPN

ACROMEGALY

AFTERCLOSUREOFTHEEPIPHYSEALPLATE


local or systemic effects

growth

large and thick hands

visual disturbances HTN

hyperglycemia

organomegaly

LAB ASST:

CT scan MRI

MEDICAL MANAGEMENT:

Transphenoidal Hypophysectomy

removal of pituitary gland

post-op: avoid sneezing

watch out for bleeding (racoonseyes, hematoma under ear). CSFleak, infection, hypopituitarism

Bromocriptine (Parlodel) SE: drowsiness

AE: fainting, depression

NURSING MANAGEMENT:

emotional support skin care prepare patient for surgery

GIGANTISM

BEFORECLOSUREOFTHEEPIPHYSEALPLATE

MEDICAL MANAGEMENT:

Octreotide Lanreotide Parlodel

Radiation therapy Surgery

SYNDROME OF INCREASED ADH

(SIADH)

HYPERSECRETIONOFADH

ETIOLOGIC CAUSES:

nonendocrine origin: bronchogeniccarcinoma

malignant lung cells synthesize andrelease ADH

severe pneumonia, pneumothorax, andother lung disorders

direct stimulation of pituitary gland

CNS disorders (head injury, brainsurgery/tumor, infection)


hypervolemia mental status change abnormal weight gain

MEDICAL MANAGEMENT:

GOAL: eliminate underlying cause

NURSING MANAGEMENT:

monitor VS, neuro status, I&O, daily

weight, provide safe environment restrict fluid intake administer diuretics (Furosemide) and

IVF carefully

with fluid restriction to treat severehyponatremia

administer prescribed Demeclemycin

ADRENAL GLANDSHYPOFUNCTIONOFADRENALGLANDS ADDISONS DISEASE

HYPERCOTISOLISM

HYPOFUNCTIONOFADRENALGLANDS

ETIOLOGIC FACTORS:

idiopathic surgical removal of both adrenal

glands infection of adrenal glands

TB, histoplasmosis inadequate secretion of ACTH therapeutic use of corticosteroids sudden cessation of ACTH therapy


muscle weakness fatigue weight loss

appetite GI disturbances

hyponatremia hypoglycemia dehydration and hypovolemia

/dark skin pigmentation anorexia emaciation (too thin) hypotension hyperkalemia mental status changes (apathy,

confusion)

NURSING MANAGEMENT:

less stress fluid monitor VS, especially BP

monitor weight monitor blood glucose level and

potassium level administer hormone agents as

prescribed (glucocorticoids)

ADDISONIANS/HYPOTENSIVE CRISIS

LIFE-THREATENING DISORDER CAUSED BY ACUTE-

SEVEREADRENALINSUFFICIENCY

CAUSES:

severe stress infection trauma/surgery

CLINICAL MANAGEMENT:


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severe headache severe abdominal pain severe weakness severe hypotension signs of shock

pallor

apprehension

rapid and weak pulse

rapid respiration

hypotension

other signs: nausea

diarrhea

cyanosis

NURSING MANAGEMENT:

administer hydrocortisone monitor VS frequently monitor I&O, neuro status, electrolyte

imbalance and blood glucose administer IVF maintain bed rest maintain antibiotics

HYPERFUNCTIONOFADRENALGLANDS

CUSHINGS DISEASE

DIURNALPATTERNOFCORTISOLISLOST

EXCESSIVEADRENOCORTICALACTIVITY

HYPERSECRETION OF GLUCOCORTICOIDS FROM

ADRENALCORTEX

ETIOLOGIC FACTORS:

adrenal tumor overuse of corticosteroids pituitary tumor ectopic production of ACTH by

malignancies

abuse of steroids DIAGNOSTIC TEST:

serum cortisol


arrest of growth obesity, musculoskeletal changes,

central-type obesitya buffalo hump in neck, heavy trunk w/

thin extremities thin and fragile skin development of bruises and striae

(ecchymoses) moon-faced kyphosis, compression fractures backache osteoporosis, muscle wasting hypertension, heart failure hyperglycemia/overt DM oiliness of skin/acne disturbed sleep lost libido mood changes visual disturbances d/t pituitary tumor slow healing of wounds weight gain

MEDICAL MANAGEMENT:

surgical removal of tumor bytransphenoidal hypophysectomy

radiation of pituitary gland adrenalectomy of primary adrena

hypertrophy

PHARMACOLOGICAL MANAGEMENT:

Metyrapone

test function of pituitary glands Mitotane

ability to stress

NURSING MANAGEMENT:

risk for injury

risk for infection prepare patient for surgery encouraging rest and activity promoting skin integrity (meticulous) improving body image

use ketonazole for production oexcess cortisol

improving thought process (foremotional instability)

monitor lab values (glucose, Na, K, Ca) administer aminoglutamide provide CHO, Na, CHON

CONNS DISEASE

HYPERALDOSTEROIDISM

MINERALOCORTICOIDS

DIAGNOSTIC TEST:

USG very serum K serum Na urinary aldosterone

NURSING MANAGEMENT:

monitor VS, I&O, USG monitor serum, K, Na provide K-rich foods administer diuretics (Spironolactone) maintain sodium-restricted diet

PHEOCHROMOCYTOMA ACTH

SECRETIONOFEPINEPHRINEANDNOREPINEPHRINEBY

MEDULLA

ADRENERGICHORMONES


hypertension severe headache palpitation tachycardia profuse sweating sweating and flushing weight loss, tremors hyperglycemia, glycosurics

NURSING MANAGEMENT:

monitor BP monitor hypertensive crisis (TOP

priority) avoid stimulation (regulate BP) administer antihypertensive (check BP) prepare phentolamine monitor blood glucose provide adequate rest caloric food prepare surgery (adrenalectomy)

depletion of water in body

monitor s/sx of shock


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IVF

lifelong glucocorticoidsreplacement

THYROID GLANDS ASSESSMENTAND DIAGNOSTIC FINDINGS

inspection and palpation

swelling and asymmetry: extend neckslightly and swallow

size, consistency, shape, symmetry, andpresence of tenderness

hands encircle patients neck

soft texture = Graves disease, firmness =Hashimotos, tenderness = thyroiditis

auscultation

localized audible vibration of a bruit = blood flow through thyroid gland(hyperthyroidism)

Serum Thyroid-Stimulating Hormone

used for monitoring thyroid hormonereplacement therapy

distinguishing disorders of thyroid andpituitary/hypothalamus

Serum Free T4 to confirm abnormal TSH

direct measurement of free thyroxine

N: 0.9 1.7ng/dL (11.5 21.8 pmol/L) Serum T3 and T4

includes protein bond and free hormonelevels that occur in response to TSHsecretion

CI: serious systemic illnesses, meds (oralcontraceptives, corticosteroids, phenytoin,salicylates), protein wasting (result ofnephrosis), androgen use

N (T4): 4.5 11.5 ug/dL (58.5 150nmol/L)

N (T3): 70 220 ng/dL (1.15 3.10nmol/L)

T3 Resin Uptake Test

indirect measure of unsaturated TBG; todetermine the amount of thyroid hormonebound to TBG and the number of availablebinding sites

useful in evaluation of thyroid hormonelevels in px who have receiveddiagnostic/therapeutic doses of iodine

free binding sites = T3 reuptake > 35% = hyperthyroidism

free binding sites = T3 reuptake < 25% = hypothyroidism

CI: estrogen, androgen, salicylates,phenytoin, anticoagulants, corticosteroids

Thyroid Antibodies

RIA techniques for antithyroid antibodies

90 % = chronic autoimmune thyroiddisease; 100 % = Hashimotos; 80% =Graves disease

Radioactive Iodine Uptake

measures rate of iodine uptake by thethyroid gland and counts the gamma raysreleased from the breakdown of iodine inthe thyroid

CI: intake of iodine

Fine-needle Aspiration Biopsy

use of small-gauge needle to samplethyroid tissue

negative = benign; positive = malignantindetermine = suspicious; inadequate =nondiagnostic

Thyroid Scan, Radioscan, Scintiscan

a scintillation detector or gamma camerawhich moves back and forth across the

area visual image is being made of the

distribution of radioactivity in the areabeing scanned

determine size, location, shape andanatomic function

hot and cold areas Serum Thyroglobulin

RIA to detect persistence or recurrence othyroid carcinoma

HYPOTHYROIDISM inadequate amount; underactive thyroid

Cretenism (children); Myxedema (adult)

TYPES:

PRIMARY/THYROIDAL

dysfunction of thyroid gland itself

SECONDARY/PITUITARY

entirely a pituitary disorder

TERTIARY/HYPOTHALMIC

disorder of the hypothalamus resultingin adequate secretion of TSH d/t stimulation of TRH

CENTRAL

failure of the pituitary gland,hypothalamus, or both

CRETENISM

thyroid deficiency present at birth

HYPOTHYROIDISM

ETIOLOGIC FACTORS:

fails to secrete several hormones medications (Lithium, iodine

compounds, anti-thyroid meds) infiltrate diseases of the thyroid atrophy of thyroid with aging iodide insufficiency and excess thyroidectomy autoimmune response radiation therapy

RISK FACTORS:

50 years above (woman) 60 years above (man) family history of thyroid problems


extreme fatigue hair loss, brittle nails, dry skin, and

numbness/tingling of fingers husky voice and hoarseness menstrual disturbances severe hypothyroidism (subnormal

temp and PR, wt gain, cachexiadebilitated states)

thickened skin, alopecia,expressionless/masklike facial features


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cold intolerance subdued emotional responses slowed speech; enlarged tongue,

hands and feet; constipation ( GI motility); possible deafness

advanced hypothyroidism: pleuraleffusion, pericardial effusion, andrespiratory muscle weakness

MEDICAL MANAGEMENT:

GOAL: restore metabolic state byreplacing missing hormone

Synthetic levothyroxine (Synthroid orLevothroid)

6 weeks

dosage is based on patients serumTSH concentration

prevention of cardiac dysfunction

long term hypothyroidism = cholesterol, atherosclerosis, andCAD

angina occurrence = oxygen needsof the myocardium exceeded itsblood supply

prevention of med interactions

may blood glucose levels; adjust insulin levels

pharma effects of digitalis glycosides, anticoagulants,indomethacim

phenytoin and tricyclicantidepressants drug effects of thyroid

bone loss and osteoporosis mayoccur

hypnotic and sedative effects maycause respiratory depression

supportive therapy

measure ABG to determine CO2

retention pulse oximetry to monitor O2

saturations

fluids are administered cautiouslyd/t danger of water intoxication

NURSING DIAGNOSIS:

alveolar ventilation leading to bradycardia

activity intolerance r/t fatigue anddepressed cognitive process

participation in activities and independence

risk for imbalanced body temp

maintenance of body temp constipation r/t depressed GI function

return to normal bowel function deficient knowledge about the

therapeutic regimen for lifelong thyroidreplacement therapy

knowledge and acceptance of theprescribed therapeutic regimen

ineffective breathing pattern r/tdepressed ventilation

improved respi status andmaintenance of normal breathingpattern

disturbed thought processes r/depressed metabolism and altered CVand respi status

improved thought process

NURSING MANAGEMENT:

avoid heating techniques calorie diet

encourage activity to constipationdrink 6-8 glasses of water; fiber-intake

maintain patient airway administer oxygen

IVF monitor I&O m

PATHOPHYSIOLOGY:

inadequate thyroid hormones

general slowing of all physical and mental

processes

general depression of most cellular enzyme

systems

metabolic activities of all cells

oxygen demand oxidation of

less body heat

nutrients

hypoxia risk for

energy hyponatremia

hyperventilation bradycardiacold intolerance

MYXEDEMA COMA

ACCUMULATION OF MUCOPOLYSACCHARIDES IN

SUBCUTANEOUSANDOTHERINTERSTITIALTISSUE

MOSTEXTREME, SEVERESTAGEOFHYPOTHYROIDISM

HIGHMORTALITY

CARBON DIOXIDE RETENTION, NARCOSIS, AND

THROIDISM

CARDIOVASCULARCOLLAPSEANDSCHOCK

INTENSIVETHERAPY IFPATIENTSURVIVE

ETIOLOGICAL FACTORS:

infection/other systemic disease use of sedatives


initially:

depression, cognitive statuslethargy, somnolence

hypotension bradycardia unresponsive hypoventilation hypovolemia convulsions hypothermia cerebral hypoxia

MEDICAL MANAGEMENT:

restore normal metabolic state byreplacing missing hormone (TSH)primary object


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oxygen therapy T4 to T3 (Cytomel); Proloid (T4 to T3)

dieresis because of edema

muscle tone

metabolic activity

slight fever

s/sx hypothyroidism in 3-12 weeks

TSH level

NURSING MANAGEMENT:

VS monitoring

administer hormone replacement calorie, cholesterol, fat manage constipation appropriately provide warm environment avoid sedatives and narcotics report chest pain promptly

HASHIMOTOS THYROIDITIS

COMMON WITH WOMEN (MULTIPLE PREGNANCY WITH

BLEEDING)

ETIOLOGIC FACTOR:

idiopathic


firm enlargement of thyroid glands

no gross nodules BMR

DIAGNOSTIC TEST:

T3, T4 normal to abnormal amounts TSH

MEDICAL MANAGEMENT:

suppression of TSH surgical resection of goiter if tracheal

compression, cough/hoarseness management of hypocalcemia

HYPERTHYROIDISM hypermetabolic condition characterized by

excessive amounts of thyroid by abnormal

stimulation of thyroid gland

HYPERTHYROIDISM :

ETIOLOGIC FACTORS:

medical conditions age gender (men are prone) genetic factors ethnic background other factors

CLINICAL MANIFESTATIONS

enlarged thyroid nervousness heat intolerance

MEDICAL MANAGEMENT: PTU and Methimazole

associated with Graves disease

SE: rash itching Radioactive iodine therapy

destroys overactive thyroid cells

common treatment in elderlypatients

hyperthyroidism will subside in 3-5weeks

Potassium Iodide, Lugols solution Beta-adrenergic blocking agents

(Propanolol)

controls nervousness

SURGICAL MANAGEMENT:

Thyroidectomy

can be all/part of the thyroid gland

patient who cannot tolerateantithyroid glands

PTU administered before surgery

Iodism iodine toxicity

NURSING MANAGEMENT:

assess cardiac respiratory function

signs for thyroid storms administer oxygen to avoid hypoxia cool, comfortable temperature improve nutritional status

reduce diarrhea provide quiet atmosphere record weight enhance coping measures

reduce stress improve self-esteem

provide eye protection

PARATHYROID GLANDS

ANATOMY-PHYSIOLOGY mobilization of Ca from bone

osteoclast activity; Ca level enhancing absorption of Ca from small

intestine

Vitamin D suppression of Ca loss in urine

rate of which Ca are loss in the urine

stimulate PO4 ions

HYPOPARATHYROIDISM inadequate parathyroid hormones

TYPES:

ACUTE iatrogenic caused by accidental damage due to

removal of parathyroid aglands

CHRONIC

idiopathic lethargy, thin, patchy hair

PSEUDOHYPOPARATHYROIDISM

Albrights hereditary osteodystrophy

HYPOPARATHYROIDISM:

ETIOLOGIC FACTORS:

occurs more in women than men


Latent tetany numbness

tingling

stiffness

cramp Overt tetany (occurs after surgery)

bronchospasm

laryngeal spasm

hypocalcemia

anxiety

irritability

depression

delirium


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ECG changes

hypotension

carpopedal spasm

dysphagia

photophobia

cardiac dysrhythmias

seizures

DIAGNOSTIC TESTS:

Positive Trosseaus sign: carpopedalspasm

use of BP cuff by applying 30-50ammHg (applying hypoxia)

result: stiffening of wrists, andadduction of fingers

Positive Chvoteks sign:

touching the earlobe

result: twitching of mouth and nose Ca levels of 5-6mg/dl or lower

PHARMACOLOGICAL MANAGEMENT:

Oral Ca Carbonate tabs Vitamin D

which can help absorb Ca andeliminate phosphorus

MEDICAL MANAGEMENT:

Parenteral Parathormone for treatment for acute

hypoparathyroidism

monitor for allergic reactions andchanges in serum level

Sedative agents for neuromuscularirritability/seizures

Aluminum hydroxide gel and Aluminumcarbonate

which should be taken after meals Phenobarbital

for seizures

NURSING MANAGEMENT:

assess client at risk numbness/tingling monitor lab values, VS, I&O administer Ca gluconate slowly and

cautiously encourage fluid intake provide health teaching Ca diet (green leafy vegetables) keep Ca gluconate and tracheostomy

set hand washing provide stress-free environment spinach is avoided (contains oxalate) Vitamin D preparation

to Ca care of post-op patient

trach set or mechanical ventilation Ca gluconate

HYPERPARATHYROIDISM excessive parathyroid secretion

TYPES:

PRIMARY

one or more parathyroid glandsaffected

SECONDARY

destruction of the one that sendsproblem dietary from cause: ricketsfrom vitamin D deficiency, chronic

renal failure, osteomalacia (d/phenytoin)

TERTIARTY

HYPERPARATHYROIDISM:


apathy, muscle weakness, n/v,constipation, hypertension, cardiacdysrythmia, cardiac contraction

musculoskeletal sx

skeletal pain/tenderness peptic ulcer and pancreatitis renal damage shortening of bone irritability renal system

polyuria

nephrocalcinosis pain in weight bearing shortening of body stature fatigue, muscle tone, muscle

weakness abdominal pain ranging to the back

ASSESSMENT:

radioimmunoassay (RIA) x-ray (bone changes) concentrations of parathormone serum Ca levels spectrophotometry ultrasound, MRI biopsy (for cysts, adenoma,

hyperplasia)

MEDICAL MANAGEMENT:

Parathyroidectomy

< 50 years old

serum Ca 1.0 mg/dl

urinary Ca level 400 mg/day

30% in renal function Mobility

bed rest is discouraged due to Caexcretion; when an individuamoves, the Ca is stored in thebones rather than in thebloodstream

Hydration therapy

2000 ml/day

cranberry juice urinary pH Diet and meds

avoid a diet with restricted/excessCa

anorexia is common

Pharmacotherapy Calcimimetic therapy

NURSING MANAGEMENT:

airway patency, dehydration,immobility, diet

fluid intake (3-4L/day) acid-ash fruit juices (prune and

cranberry juice) protect from injury to prevent fracture NS IV ( Na)

Ca excretion is promoted by Naexcretion

mobility


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bed rest Ca diet/meds

Ca diet

administer antacids those withpeptic ulcer

thiazide diuretics must be avoided(as it promotes Ca reabsorption)

endo alterations

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