the parathyroid glands-edited

8/6/2019 The Parathyroid Glands-edited

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THE

PARATHYROIDGLANDS



Anatomic and Physiologic Overview



HYPERPARATHYROIDISM

caused by overproduction of

parathormone characterized by bone

decalcification & development of renal calculi containing

Calcium

Specific Disorders of the

Parathyroid Glands



Types of Hyperparathyroidism

a. Primary hyperparathyroidism

hyperplasia or tumor of one of the

parathyroid glandsb. Secondary hyperparathyroidism

gland enlargement due to chronic

hypocalcemia



c. Tertiary hyperparathyroidism

parathyroid glands are enlarged & do

not respond to changes in serum Ca

levels, usually associated w/ chronic

renal failure

Types of Hyperparathyroidism



Clinical Manifestations

� May be asymptomatic/symptomatic

� Apathy

�

Fatigue� Muscle weakness

� n/v

� Constipation

� HPN

�

Cardiac dysrhythmias



Increase in Ca produces a decrease inexcitation potential of nerve and muscle tissue

Formation of renal stones r/t increased urinaryexcretion of Ca & Ph, occurs in 55% of pts. w/primary hyperparathyroidism

Renal damage results from the precipitation of

Ca phosphate in the renal pelvis &parenchyma, w/c causes renal calculi,obstruction, pyelonephritis, & renal failure



Assessment & Diagnostic Findings

P rimary hyperparathyroidism is

diagnosed by persistent elevation of

serum calcium levels & elevatedconcentration of parathormone

RIA for parathormone are sensitive &

differentiate primaryhyperparathyroidism from other causes

of hypercalcemia



Double-antibody parathyroid hormone test

is used to distinguish b/w primaryhyperparathyroidism & malignancy as a

cause of hypercalcemia

UTZ, MRI , Thallium scan, & fine-needle

biopsy used to evaluate the function of

the parathyroids & to localize theparathyroid cysts, adenomas, or

hyperplasia



Medical Management

Recommended treatment of primary

hyperparathyroidism is surgical removal

of abnormal parathyroid tissue(parathyroidectomy)



Hydration therapy

daily fluid intake of 2000 ml or

more is encouraged

cranberry juice lowers urinary

pHavoid thiazide diuretics - decrease

renal excretion of Ca &

further elevate serum Calevels

(hypercalcemic crisis) instruct to

avoid dehydration



Mobility

walking or use of a rocking chair (for

those w/ limited mobility)

bones that are subjected to

normal stress give up less Ca

avoid bed rest increases Ca excretion

& risk for renal calculi

oral phosphatase lower the serum

Ca level, long-term use is not

recommended because of risk of

ectopic Ca phosphate deposition

in soft tissues



Diet & Medications

avoid diet w/ restricted or excess Ca(if w/ coexisitng peptic ulcer)

antacids & CHON feedings

anorexia improve appetite

constipation prune juice, stool

softeners, & physical activity,

increase fluid intake(common post-operatively)



Nursing Management

� Awareness of the course of the disorder

& an understanding approach by the

nurse may help the patient and familydeal with their reactions & feelings

� close monitoring for life-threateningcomplications of the tx



Complications: Hypercalcemic crisis

� Characterized by extreme elevation of

serum Ca levels >15 mg/dl (3.7 mmol/L)

result in neurologic, cardiovascular & renal

symptoms

tx: rehydration, diuretic agents to promote

renal excretion of excess Ca, & phosphate

therapy to correct hypophosphatemia &

decrease serum Ca levels by promoting Ca

deposition in bone & reducing GI

absorption of Ca



� Cytotoxic agents (mithramycin),

calcitonin, & dialysis may be used inemergency situations to decrease serum

Ca levels quickly

�

combination of calcitonin &corticosteroids (in emergencies) to

reduce serum Ca level by increasing Ca

deposition in bone� biphosphonates etidronate,

pamidronate to dec serum Ca levels



HYPOPARATHYROIDISM

inadequate secretion of parathormone

after interruption of the blood supply or

surgical removal of parathyroid gland

tissue during thyroidectomy,

parathyroidectomy, or radical neck

dissection

results in increased blood phosphate

(hyperphosphatemia) and decreased

blood Ca levels



In the absence of parathormone, there is

decreased intestinal absorption of dietary Ca

& decreased resorption of Ca from bone &

through the renal tubules

Decreased renal excretion of phosphate causes

hypophosphaturia, & low serum Ca levelsresult in hypocalciuria




(+) trousseaus sign is positive when

carpopedal spasm is induced by

occluding the blood flow to the arm for 3minutes w/ BP cuff

(+) Chvosteks sign is positive when a

sharp tapping over the facial nerve just infront of the parotid gland & anterior to

the ear causes spasm or twitching of the

mouth, nose & eye



�

Tetany develops at serum Ca levels of 5 to 6 mg/dl (1.2 to 1.5 mmol/L) or

lower

� Serum Ph increased

� X-ray of bone increased density;

calcification of the subcutaneous orparaspinal basal ganglia of the brain



Medical Management

�

Goal of therapy: to increase s. Ca level to9-10 mg/dl (2.2-2.5 mmol/L) & eliminate

symptoms of hypoparathyroidism &

hypocalcemia� Administration of IV Calcium gluconate,

sedative agents (pentobarbital)

� Parenteral parathormone to tx acutehypoparatyhroidism w/ tetany;

monitored for allergic reactions



� Environment: free of noise, drafts, bright

lights, or sudden movement

� Tracheostomy or mechanical ventilation,

bronchodilating medications for

respiratory distress� Oral tabs Ca gluconate

Al H3O gel/Al CO3 (Gelusil, Amphojel)

administered after meals to bindphosphate & promote its excretion

through the GIT



� Vit. D preps enhance Ca absorption

from GIT



Nursing Management

Care of postoperative pts detectingearly signs of hypocalcemia &

anticipating signs of tetany, seizures, &

respiratory difficulties Ca gluconate kept at bedside, w/

equipment necessary for IV

administration; caution w/ pt w/ cardiacd/o & is receiving digitalis, given slowly &

cautiously (inc. systolic contraction)



THEADRENALGLANDS

Anatomic & Physiologic Overview



Anatomic & Physiologic Overview

� Adrenal medulla function as part of the

ANS

stimulation of preganglionic sympatheticnerve fibers, w/c travel directly to the

cells of the adrenal medulla, causes

release of the catecholamine hormonesepi & norepi

- regulates catabolism of stored fuels to

meet caloric needs



- prepares the body to meet a challenge

(fight-or-flight response)- causes decreased blood flow to tissues

that are not needed in emergency

situations (GIT) (cardiac/skeletal muscle- induce release of free fatty acid,

increase BMR, & elevate blood glucose

level



� Adrenal Cortex makes it possible to

adapt to stress of all kinds

w/o this, severe stress would cause

peripheral circulatory failure, circulatory

shock & prostration Glucocorticoids are so-called for

their influence on glucose metabolism:

increased hydrocortisone secretion(elevates bld. glucose level)



- inhibit inflammatory response to tissue

injury & suppress allergic manifestation

- S/E: devt of DM, osteoporosis, peptic

ulcer, increased protein breakdown

resulting in muscle wasting & poorwound healing, & redistribution of body

fat



Mineralocorticoids:

� Has major effect in electrolytemetabolism

� Act on renal tubular & GI epithelium to

cause increased Na ion absorption inexchange for excretion of K or

Hydrogen ions



Adrenal Sex Hormone ( Androgens)

�

devt of secondary characteristics� stimulate protein synthesis and inhibit

protein breakdown, enhancing the

growth of muscle and bone tissue inthe developing male

� May also secrete small amounts of

male & female sex hormones



Adrenocortical Insufficiency

(Addisons Disease)

Occurs when adrenal cortex function is

inadequate to meet the pts need for

cortical hormones

Autoimmune or idiopathic atrophy

Surgical removal of both adrenal glands& infection of AG (TB & histoplasmosis)



Inadequate secretion of ACTH = dec.

stimulation of AC Use of corticosteroids (suppress

function of adrenal cortex)



Clinical Manifestations

� Muscle weakness, anorexia, GI

symptoms, fatigue, emaciation, dark

pigmentation of the mucous membrane& the skin (knuckles, knees, & elbows),

hypotension, low bld. Glucose, low s. Na,

high s. K levels� mental status changes: depression,

emotional lability, apathy, & confusion



� w/ disease progression & acute

hypotension, addisonian crisis develops

� Characterized by cyanosis, classis signs of

circulatory shock: Pallor, apprehension,

rapid & weak pulse, rapid respirations, &

low BP

� h/a, nausea, abd. Pain, diarrhea

confusion, restlessness




� Early morning serum cortisol (<165

nmol/L) & plasma ACTH

� Primary insufficiency (>22.0 pmol/L)

� Decreased levels of glucose & Na, Inc.

level of K & inc. WBC count

� Confirmed by low levels of adrenocortical

hormones in the blood or urine &

decreased serum cortisol levels



Medical Management

� Administering fluids & corticosteroids,

monitoring v/s, placing pt in recumbent

position� Hydrocortisone (Solu-Cortef) given IV

followed by 5% dextrose in NS

� Vasopressor for hypotension (persistent)

� Antibiotics



Nursing Management

� Assess the patient especially BP & PR,

skin color/turgor, wt changes, muscle

weakness, fatigue, precipitating factor� Monitoring & Managing Addisonian Crisis

� Monitor s/s indicative of Addisonian

crisis: Shock



� Avoid physical & psychological stressors

(avoiding overexertion, cold, infection,emotional distress)

� IV administration of fluid, glucose,

electrolytes (Na), replacement of missingsteroid hormones, vasopressors



Restoring Fluid Balance

Improve Activity Tolerance

- maintain a quiet, non-stressful envt

P romoting home & community-based care- teaching patients self-care explicit

verbal & written instructions how &

when to use the injection, inform otherhealth care providers, wearing a medic

alert bracelet, & carry information at all

times about the need for corticosteroids



- need to know the signs of excessive orinsufficient hormone replacement

Continuing care

Referral for home care to assess ptsrecovery, monitor hormone replacement,& evaluate stress in the home, assess thept & familys knowledge about the

medication therapy & dietarymodifications

the parathyroid glands-edited

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