ENDOCRINESYSTEM

By: MISS SHENELL A. DELFIN, RN

FUNCTION:Endocrine system consist of a series of glands

that function individually or conjointly to integrate and control innumerable metabolic activities in the body.

These glands automatically regulate various body processes by releasing chemical signals called hormones.

FUNCTION:Maintenance and regulation of vital functions.Response to stress or injuryGrowth and developmentReproductionFluids and electrolytesAcid base-balanceEnergy metabolism

ENDOCRINE GLANDSENDOCRINE GLAND

HORMONES FUNCTIONS

PITUITARY

ANTERIOR

TSH Thyroid to release hormones

LOBE ACTH Adrenal cortex to release hormones

FSH,LH Growth, maturation & function of sex organs

GH/

SOMATOTROPIN

Growth of body tissues & bones

PROLACTIN/

LTH

Development of mammary glands & lactation

ENDOCRINE GLANDSENDOCRINE GLAND

HORMONE FUNCTION

PITUITARY

POSTERIOR

LOBE

ADH Regulates water metabolism

OXYTOCIN Stimulate uterine contractions

release of milk

INTERME-

DIATE LOBE

MSH Affects skin pigmentation

ENDOCRINE GLANDSENDOCRINE GLAND

HORMONES FUNCTION

ADRENAL CORTEX

ALDOSTERONE Fluid & electrolyte balance;

Na reabsorption;

K excretion

CORTISOL Glycogenolysis;

Gluconeogenesis

Na & water reabsorption

Antiinflammatory

Stress hormone

SEX

HORMONES

Slightly significant

ENDOCRINE GLANDS

ENDOCRINE

GLAND

HORMONE FUNCTION

ADRENAL MEDULLA

EPINEPHRINE

NOR-

EPINEPHRINE

Increase heart rate & BP

Bronchodilation,

Glycogenolysis

Stress hormone

ENDOCRINE GLANDSENDOCRINE GLAND

HORMONE FUNCTION

THYROID T3 & T4’ Regulate metabolic rate

Regulate physical & mental growth & development

THYRO-

CALCITONIN

Decrease serum Ca by increasing bone deposition

PARA-

THYROID

PTH Increase serum calcium by promoting bone decalcification

ENDOCRINE GLANDSENDOCRINE

GLAND

HORMONE FUNCTION

PANCREAS

BETA

CELLS

INSULIN Decrease blood glucose by:

Glucose diffusion across cell membrane;

Converts glucose to glycogen

ALPHA

CELLS

GLUCAGON Increase blood glucose by:

Gluconeogenesis

Glycogenolysis

ENDOCRINE GLANDSENDOCRINE

GLAND

HORMONES FUNCTION

OVARIES ESTROGEN &

PROGES-

TERONE

Development of secondary sex charac in female

Maturation of sex organs

Sexual functioning

Maintenance of pregnancy

TESTES TESTOS-

TERONE

Development of secondary sex charac in male

Maturation of sex organs

Sexual functioning

HORMONE REGULATIONNEGATIVE FEEDBACK MECHANISM

CHANGING OF BLOOD LEVELS OF CERTAIN SUBSTANCES (e..g CALCIUM & GLUCOSE)

RHYTHMIC PATTERNS OF SECRETION (e.g. CORTISOL, FEMALE REPRODUCTIVE HORMONES)

AUTONOMIC & C.N.S. CONTROL(PITUITARY-HYPOTHALAMIC AXIS,

ADRENAL MEDULLA HORMONES)

NEGATIVE FEEDBACK MECHANISM

DECREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine)

PITUITARY GLAND RELEASE OF STIMULATING HORMONE (e.g. TSH)

STIMULATION OF TARGET ORGANS TO PRODUCE & RELEASE HORMONE

(e.g. Thyroid gland release of Thyroxine)

RETURN OF THE NORMAL CONCENTRATION OF HORMONE

NEGATIVE FEEDBACK MECHANISM

INCREASED HORMONE CONCENTRATION IN THE BLOOD (e.g. Thyroxine)

PITUITARY GLAND IS INHIBITED TORELEASE STIMULATING HORMONE (e.g. TSH)

DECREASED PRODUCTION & SECRETION OF TARGET ORGAN OF THE HORMONE

(e.g. Thyroid gland release of Thyroxine)

RETURN OF THE NORMAL CONCENTRATION OF HORMONE

Hypothyroidism underactive state of the thyroid gland

hyposecretion of thyroid hormone most common in women, middle-age primary function is to control the level of cellular

metabolism by secreting thyroxin (T4) and triiodothyronine (T3)Causes :

thyroidectomy pituitary / hypothalamic dysfunction iodine deficiency autoimmune thyroiditis (Hashimoto’s disease) –

immune system attacks the thyroid gland idiopathic (unknown)

DX: decreased T3, T4 Elevated TSH, cholesterol

Med. Mgt. – thyroid replacement therapy Levothyroxine (Synthyroid) , liothyronine Expected effects: diuresis, puffiness, improved

reflexes and muscle tone, PRNsg. Interventions

provide a warm environment, conducive to rest avoid use of all sedatives assist client in choosing calorie, cholesterol

diet fluid and fiber to relieve constipation physical activity and sensory stimulation gradually as condition improves monitor cardiovascular response to increased

hormone levels carefully provide info. about prescribed medications (name, dosage, side effects) and importance of lifelong medical supervision

Hyperthyroidism

over-secretion of the thyroid gland also called thyrotoxicosis or graves disease,

tissues are stimulated by excessive thyroid hormone

a recurrent syndrome, may appear after emotional stress or infection

occurs mostly in women 20-50 yrs old

Causes : adenoma, goiter, viral inflammation, auto-immune glandular stimulation, grave’s disease - most common cause

Hyperthyroidism (cont.)

DX: > elevated T3, T4 valuesT4= 5-12mcg/dl , T3= 70-220 ng/dl , TSH= 0.2-5.4 mU/L•abnormal findings in the thyroid scan

Goiter – enlargement of the thyroid gland •due to stimulation of the thyroid gland by TSH

Simple goiter – enlarged thyroid gland•due to iodine deficiency, intake of goitrogenic foods cabbage, turnips, soybeans•may be hereditary

Grave’s Disease disorder char. by one or more of the ff:

diffuse goiter

hyperthyroidism

infiltrative opthalmopathy exophthalmos seen in females under age 40 result from stimulation of the thyroid gland by thyroid-stimulating immunoglobulins (TSI) cause is unknown, may be hereditary, gender-related, often occurs after severe emotional stress or infection

Thyroid Storm or Crisis

a medical emergency pts. develop severe manifestation of hyperthyroidism

temp., tachycardia, dysrhythmias worsening tremors, restlessness delirious or psychotic state or coma abdominal pain BP and RR

Precipitated by a major stressor: infection trauma or surgery (thyroidectomy) inadequate treatment

Complications :

cardiovascular disease (HPN, Angina, CHF) Exophthalmos – abnormal protrusion of the

eyeballs- caused by abnormal deposits of fat and fluid in the retroocular tissue

Corneal abrasion Thyroid storm or crisis life-threatening

hypermetabolism and excessive adrenergic response (HR, RR, BP)

TAKE ME! TAKE ME!!

Anxiety Flushed, smooth skin Heat intolerance Mood swings Diaphoresis Tachycardia Palpitations Dyspnea Weakness Wt. loss

Assessment Findings

Nsg. Interventions: Provide calm, restful envt. Provide calm, restful envt.

1. physical comfort, cool envt. temp., bathe frequently w/ cool water

2. provide adequate rest, avoid muscle fatigue33 stressors in the envt.— noise and lights4. relaxation techniques

Provide adequate nutrientsProvide adequate nutrients33 calorie, protein, balanced diet (4,000-

5,000 cal/day)33 fluid intake3. Restrict stimulants (tea, coffee, alcohol)4. small, frequent feedings if hypermotility is

present5. Daily wt.

Nsg. Interventions:

Provide emotional supportProvide emotional support

Provide eye careProvide eye care1. eye drops, dark glasses, patch eyes if

necessary2. elevate head of bed for sleep3. restrict dietary sodium4. assess adequacy of lid closure

Be alert for complicationsBe alert for complications

Post-op care after Thyroidectomy

O2 therapy, suction secretions Monitor for signs of bleeding and excessive edema elevate head of bed 30o, support head and neck – to avoid tension on suturescheck dressing frequently, check behind the neck for bleeding assess for signs of resp. distress, hoarseness (laryngeal edema or damage) keep tracheostomy set in patient’s room for emergency use

Post-op Complications: be alert for the possibility of:

1. Tetany (due to hypocalcemia caused by accidental removal of parathyroid glands)

assess for numbness, tingling or muscle twitching Chvostek’s sign and Trousseau’s sign Ca+ gluconate IV

2. HemorrhageWOF: hypotension, tachycardia, other signs of hypovolemiaWOF: irregular breathing, swelling, choking---possible hemorrhage and tracheal compressionWOF: early signs of hemorrhage: repeated clearing of the throat, difficulty swallowing

Post-op Complications: be alert for the possibility of:

3. Thyroid storm - life-threatening- sudden release of thyroid hormone- fever, tachycardia, increasing restlessness

and agitation, delirium

administer food and fluid with care (dysphagia is common) encourage client to gradually ROM of neckteach about medications, frequent follow-up

total thyroidectomy – life long replacement medication (T3, T4)subtotal thyroidectomy – careful monitoring of return of thyroid function

(TYPE I, TYPE II)

Diabetes MellitusDiabetes Mellitus

is a chronic disorder of carbohydrate, protein, and fat metabolism resulting from insulin deficiency or abnormality in the use of insulin

Predisposing factors: exact cause of diabetes mellitus remain unknown genetic / hereditary predisposition viruses pancreatitis pancreatic tumor autoimmune disorder obesity (overweight people require more insulin to metabolize the food they eat or the number of insulin receptor sites in cells is decreased)

Types1.Insulin – Dependent Diabetes Mellitus (IDDM) or Type I

destruction of beta cells of the pancreas little or no insulin production requires daily insulin admin. may occur at any age, usually appears below age 15

2.Non Insulin–Dependent Diabetes Mellitus (NIDDM) or Type II

probably caused by:1. disturbance in insulin reception in the cells2. number of insulin receptors3. loss of beta cell responsiveness to glucose leading to slow or insulin release by the pancreas

occurs over age 40 but can occur in children common in overweight or obese w/ some circulating insulin present, often do not require insulin

Clinical Manifestations ( Signs and Symptoms)

- Polyuria - weakness- Polydipsia - fatigue- Polyphagia - blood sugar / glucose level- weight loss - (+) glucose in urine (glycosuria)- nausea / vomiting - changes in LOC (severe hyperglycemia) (sleepiness, drowsiness coma)- recurrent infection, prolonged wound healing- altered immune and inflammatory response, prone to infection (glucose inhibits the phagocytic action of WBC resistance)- genital pruritus – (hyperglycemia and glycosuria favor fungal growth : candidal infection – resulting in pruritus, common presenting symptom in women)

1. Fasting Blood Sugar (FBS) NPO for 12 hours Normal value= 80-120 mg/dl 140 mg/dl or more – diagnostic of DM

2. Postprandial blood sugar Blood is withdrawn 2 hrs. after a meal N value = < 120mg/dl 200 mg/dl or more is diagnostic of DM

3. Oral Glucose Tolerance Test (OGTT) NPO 12 hrs, no smoking, coffee or tea, minimize

activity, minimize stress obtain FBS, administer 100 gm. Glucose by mouth

diluted in juice; obtain blood and urine specimen after 1, 2 and 3 hrs.

N value = blood glucose rise to 140 mg/dl in the 1st hour and returns to normal by 2nd and 3rd hrs.

Abnormal = blood glucose does not return to normal by 2nd and 3rd hrs.; all urine specimen positive for glucose

4. Glycosylated hemoglobin Provides information about blood glucose

level during the previous 3 months bec. glucose in the bloodstream attaches to

some of the hemoglobin and stay attached during the 120-day lifespan of the RBC

Interventions for Diabetes MellitusA.Dietary Management

1. Follow individualized meal plan and snacks as scheduled Balanced diabetic diet – 50% CHO, 30% fats,

20% CHON, vitamins and minerals diet based on pts. size, wt., age, occupation and

activity2. Pt. must have adequate CHO intake to correspond to

the time when insulin is most effective• Routine blood glucose testing before each meal and

at bedtime is necessary during initial control, during illness and in unstable pts.

• Do not skip meals• Measure foods accurately, do not estimate • Less added fat, fewer fatty foods and low-cholesterol

Interventions for Diabetes MellitusA.Dietary Management

7. Advise use of complex carbohydrates to help stabilize blood sugar. Meal should include more fiber and starch and fewer simple or refined sugars.

8. Avoid concentrated sweets, high in sugar (jellies, jams, cakes, ice cream)

9. If taking insulin, eat extra food before periods of vigorous exercise

10.Avoid periods of fasting and feasting

11.Keep weight at normal level, obese diabetics should be on a strict weight control program and should lose weight.

B. Teach pt. on correct administration of insulin and other hypoglycemic agents.

1. insulin in current use may be stored at room temp., all others in ref. or cool area

2. avoid injecting cold insulin lead to tissue reaction3. roll insulin vial to mix, do not shake, remove air

bubbles from syringe4. press (do not rub) the site after injection (rubbing

may alter the rate of absorption of insulin)5. avoid smoking for 30 mins. after injection (cigarette

smoking absorption)6. Rotate sites7. Failure to rotate sites may lead to Lipodystrophy8. Lipodystrophy – localized disturbance of fat

metabolism9. Ex. Lipohypertrophy – thickening of subcutaneous

tissue at injection site, feel lumpy or hard, spongy result to absorption of insulin making it

difficult to control the pt.’s blood glucose

Factors that influence the body’s need for Factors that influence the body’s need for insulininsulin33 need : trauma, infection, fever, severe psychological or physical stress, other illnesses2. need : active exerciseHypoglycemiaHypoglycemia

low blood glucose (usually below 60mg/dl) results from too much insulin, not enough food,

and/or excessive physical activity may occur 1-3 hrs after regular insulin injection

S/Sx:1.Sweating, tremor, pallor, tachycardia, palpitations and nervousness

caused by release of epinephrine from the CNS when blood glucose falls rapidly

2.Headache, light-headedness, confusion, numbness of lips and tongue, slurred speech, drowsiness, convulsions and coma

• caused by depression of the CNS because of glucose supply of brain cells

Management of Hypoglycemia

1.Give simple sugar orally if pt. is conscious and can swallow – orange juice, candy, glucose tablets, lump of sugar2.Give Glucagon (SQ or IM) if pt. is unconscious or cannot take sugar by mouth3.As soon as pt. regains consciousness, he should be given carbohydrate by mouth4.If pt. does not respond to the above measures, he is given 50 ml of 50% glucose I.V. or 1000 ml of 5%-10% glucose in water I.V.

Preventing Hypoglycemic Reactions Due to Insulin

Instruct the pt. as follows:1.Hypoglycemia may be prevented by maintaining regular exercise, diet and insulin2.Early symptoms of hypoglycemia should by recognized and treated3.Carry at all times some form of simple carbohydrate (orange juice, sugar, candy)4.Extra food should be taken before unusual physical activity or prolonged periods of exercise5.Between-meal and bedtime snacks may be necessary to maintain a normal glucose level.

D-I-A-B-E-T-E-SD-I-A-B-E-T-E-SD-D- DIET: 50-60% CHO, 20-30% FATS, 10-

20% CHONI-I- INSULIN– TYPE 1A-A- ANTIDIABETIC AGENTS– TYPE 2B-B- BLOOD SUGAR MONITORINGE- E- EXERCISET-T- TRANSPLANT OF PANCREASE-E- ENSURE ADEQUATE FOOD INTAKES- S- SCRUPULOUS FOOT CARE

Oral Antidiabetic AgentsOral Antidiabetic Agents

INSULIN THERAPYDISPENSED IN “U”/ml : eg 100, 80REFRIGERATEGIVEN @ ROOM TEMPGENTLY ROTATED, NOT SHAKENROUTE : SQ ; IM OR IV SYRINGE: 5/8 INCH ; SAME BRAND

INSULIN ONSET PEAK DURATION

Ultra rapid acting Insulin analog (Humalog)

15 mins. 2-4 hrs. 6-8 hrs.

Rapid acting: Regular (Semilente)

½-1 hr 2-4 hrs. 6-8 hrs.

Intermediate: NPH (Lente)

1-2 hrs. 7-12 hrs. 24-30 hrs.

Long acting: Protamine Zinc (Ultralente)

4-6 hrs. 18 + hrs 30-36 hrs.

INSULIN THERAPY:SITE OF INJECTION:

ABDOMENANTERIOR THIGHARM UPPER BACK BUTTOCKS

LIPODYSTROPHY

CAUSE:FAULTY TECHNIQUETRAUMAINJECTION OF REFRIGERATED INSULIN

MANAGEMENT:ROTATING SITES: 1 AREA IS NOT USED MORE

THAN ONCE EVERY 3 WKS

Teach pt. to estabilish and maintain a pattern of regular exercise Benefits of exercise :

promotes use of CHO & enhances action of insulin blood glucose levels need for insulin the no. of functioning receptor sites for insulin

perform exercise after meals to ensure an adequate level of blood glucosecarry a rapid-acting source of glucose during exerciseexcessive or unplanned exercise may trigger hypoglycemiatake insulin and food before active exercise

Teach pt. to practice good personal hygiene and positive health promotion to avoid diabetic complications

1.teach pt. about diabetic foot care2.teach pt. the adjustments that must be made in the event of minor illness (e.g. colds, flu)

continue taking insulin or oral hypoglycemic agents maintain fluid intake frequency of blood testing or urine testing

3.help pt. identify stressful situations in lifestyle that might interfere with good diabetic control4.encourage good daily hygiene5.advise regular eye exams6.teach aggressive care for minor skin cuts and abrasions

DIABETIC KETO-ACIDOSIS (DKA)

INSULIN SHOCK

HYPERGLYCEMIC, HYPEROSMOLAR, NONKETOTIC (HHONK) COMA

Diabetic Ketoacidosis (DKA) Coma

S/Sx:polyuria, thirstnausea, vomiting, abdominal pain –-- due to

acidosisweakness, headache, fatigue --- due to acidosis and

F/E imbalancedim visiondehydration, hypovolemic shock (PR, BP, dry

skin, wt. loss)hyperpnea (Kussmaul’s breathing)acetone breath (fruity odor)lethargy COMABlood glucose level > 250-350 mg/100 ml.

INSULIN SHOCKLOW BLOOD SUGAR

CAUSE:OVERDOSE OF EXOGENOUS INSULIN

EATING LESS

OVEREXERTION WITHOUT ADDITIONAL CALORIE INTAKE

INSULIN SHOCKS/SX:PARASYMPATHETIC

HUNGERNAUSEAHYPOTENSIONBRADYCARDIA

CEREBRALLETHARGY,YAWNINGSENSORIUM CX

SYMPATHETICIRRITABILITYSWEATINGTREMBLINGTACHYCARDIAPALLOR

INSULIN SHOCKCLINICAL FINDING : BLOOD GLUCOSE BELOW 55-60 mg/DL

TREATMENT:GLUCOSE PO ( SUGAR, ORANGE JUICE OR

CANDY) or IVADMINISTRATION OF GLUCAGON IM, IV OR

SQ

Hyperglycemic, Hyperosmolar, Non-Ketotic Coma (HHNC)

can occur when the action of insulin is severely inhibitedseen in pts. w/ NIDDM, elderly persons w/ NIDDM

Precipitating factors:infection, renal failure, MI, CVA, GI hemorrhage,

pancreatitis, CHF, TPN, surgery, dialysis, steroids

S/Sx:polyuria oliguria (renal insufficiency)lethargytemp, PR, BP, signs of severe fluid deficitConfusion, seizure, comaBlood glucose level > 600 mg/100 ml.

HHONKS/SX:S/SX OF DKA WITHOUT:

KAUSMAUL’S BREATHINGACETONE BREATHMETABOLIC ACIDOSISKETONURIA

LACTIC ACIDOSIS

SEVERE TISSUE ANOXIASEVERE TISSUE ANOXIA

LACTIC ACID PRODUCTIONLACTIC ACID PRODUCTION

AGGRAVATION OF EXISTINGMETABOLIC ACIDOSIS

AGGRAVATION OF EXISTINGMETABOLIC ACIDOSIS

Interventions for DKA and Hyperosmolar Coma

Regular insulin IV push or IV drip 0.9% NaCl IV – 1 L during the 1st hr, 2-8 L over 24

hrs. administer sodium bicarbonate IV to correct acidosis Monitor electrolyte levels, esp. serum K+ levels administer K+, monitor UO hourly (30ml/hr)

Long-term Complications of DM

1.Vascular Changesa.) Macroangiopathy – hardening and damage of the walls of large arteries

Coronary Artery DiseaseCVA (Stroke)Peripheral vascular disease – foot ulcers and gangrene

b. ) Microangiopathy – destruction of small blood vesselsRetinopathy – damage to retinal capillaries; hemorrhage, blindnessNephropathy – damage microcirculation of kidneys; CRF

2. Neuropathy Damage to the neurons caused by vascular insufficiency and blood glucoseSensory and motor impairmentNumbness, tingling, pain in extremities Painless neuropathy

Impotence!!

SURPRISE!!!

PARATHYROID GLAND4 GLANDSSECRETES PARATHORMONE (PTH) IN

RESPONSE TO SERUM Ca & Ph LEVELSREGULATE CALCIUM & PHOSPHORUS

METABOLISMORGANS AFFECTED:BONES - RESORPTIONKIDNEYS

Ca REABSORPTIONPh EXCRETION

GIT – ENHANCES Ca ABSORPTION

Hypoparathyroidism is characterized by decrease in

the PTH level

Mobilization of calcium and phosphorous

from bone

Promotes resorption of calcium from

bone to maintain normal serum calcium levels

Promotes absorption of calcium in the GI tract ( by stimulating kidneys to convert vit.D to its active form).

Renal: increases calcium

reabsorption and phosphate excretion

Function of calcium: maintains N muscle and neuromuscular responses.Necessary component for blood coagulation mechanisms

CALCIUM STAYS IN THE BONE

CALCIUM DEPOSITED

IN THE BONE

EXCRETION OF CALCIUM

HYPOCALCEMIA

•TINGLING OF FINGERS•CHVOSTEKS/ TROUSSEAU’S•FATIGUE, WEAKNESS•CARDIAC ARRHYTHMIAS•SEIZURE•BRONCHOSPASM

HYPOPARATHYROIDISMDECREASED PTH PRODUCTIONHYPOCALCEMIA CALCIUM IS:

DEPOSITED IN THE BONE EXCRETED

CAUSE:HEREDITARYIDIOPATHICSURGICAL

PARATHYROID DISORDERS

DIAGNOSTIC TESTS:HEMATOLOGICAL

SERUM CALCIUMSERUM PHOSPHORUSSERUM ALKALINE PHOSPHATASE

URINARY STUDIESURINARY CALCIUMURINARY PHOSPHATE - TUBULAR

REABSORPTION OF PHOSPHATE

HYPOPARATHYROIDISMS/SX:ACUTE HYPOCALCEMIA

TINGLING OF THE FINGERSCHVOSTEK’S, TROUSSEAU’S

CHRONIC HYPOCALCEMIAFATIGUE, WEAKNESSPERSONALITY CHANGESLOSS OF TOOTH ENAMEL, DRY SCALY SKINCARDIAC ARRHYTHMIACATARACT

HYPOPARATHYROIDISMXRAY: INCREASED BONE DENSITYMANAGEMENT:Ca SUPPLEMENTVIT D SUPPLEMENT – LIQ FORM: WITH WATER,

JUICE OR MILK, pc

SEIZURE precLISTEN FOR STRIDOR OR HOARSENESSTRACHEOSTOMY SET @ BEDSIDE

CaGLUCONATE @ BEDSIDE

Hyperparathyroidism is characterized by excesssive

secretion of PTH

Mobilization of calcium and phosphorous

from bone

Promotes resorption of calcium from

bone to maintain normal serum calcium levels

Promotes absorption of calcium in the GI tract ( by stimulating kidneys to convert vit.D to its active form).

Renal: increases calcium

reabsorption and phosphate excretion

Function of calcium: maintains N muscle

and neuromuscular responses.

Necessary component for blood coagulation

mechanisms

CALCIUM RELEASED INTO

THE BLOOD LEADS TO BONE

DAMAGE

HYPERCALCEMIA, LACK OF RESORPTION OF CALCIUM INTO THE

BONE( BONE CYST AND PATHOLOGIC

FRACTURE)

TUBULAR CALCIUM DEPOSIT- KIDNEY

STONES, AZOTEMIA, HPN BY RF, RENAL

FAILURE

ANOREXIAN/V

CONSTIPATIONPEPTIC ULCER DSE

MUSCLE WEAKNESS

PERSONALITY CHANGESCARDIAC

ARRHYTHMIAS

HYPERPARATHYROIDISMINCREASED PTH PRODUCTIONHYPERCALCEMIAHYPOPHOSPHATEMIAPRIMARY – TUMOR OR HYPERPLASIA OF THE

PARATHYROID GLAND

SECONDARY – COMPENSATORY OVERSECRETION OF PTH IN RESPONSE TO HYPOCALCEMIA FROM:CHRONIC RENAL DSERICKETSMALABSORPTION SYNDROMEOSTEOMALACIA

HYPERPARATHYROIDISMS/SX:

BONE PAIN : ESP @ THE BACK, PATHOLOGIC FRACTURES

TUBULAR CALCIUM DEPOSITS - KIDNEY STONES, RENAL COLIC, POLYURIA, POLYDIPSIA

MUSCLE WEAKNESSPERSONALITY CX, DEPRESSIONCARDIAC ARRHYTHMIAS, HPN

XRAY: BONE DEMINERALIZATION

HYPERPARATHYROIDISMMANAGEMENT:

TX OF CHOICE : SURGICAL REMOVAL OF HYERPLASTIC TISSUE

IV PNSS 5L/ DAY WITH DIURETICSCRANBERRY JUICE (ACID-ASH)LOW Ca, HIGH Ph DIET NO MILK, CAULIFLOWER & MOLASSESSTRAIN URINE FOR STONESCARE FOR PARATHYROIDECTOMY

ADRENAL GLANDSTIMULATED BY ACTHADRENAL MEDULLA- ADRENAL MEDULLA- SECRETES

CATECOLAMINE, EPINEPHRINE, & NOREPINEPHRINE.

ADRENAL CORTEX- ADRENAL CORTEX- MAIN BODY; RESP FOR SECRETION OF GLUCO,MINERALO, SEX HORMONES (ANDRO & ESTRO)

FUNCTION IS TO CONTROL THE (-) CONTROL THE (-) FEEDBACK MECHANISMS FEEDBACK MECHANISMS REGULATING HORMONE RELEASE

ADRENAL GLANDHORMONE FUNCTION

ALDOSTERONE Renal : Na & Cl reabsorption; K excretion

GI : Na absorption

GLUCO-

CORTICOIDS

increase serum glucose by gluconeogenesis & glycogenolysis esp during STRESS

Blocks inflammation

Counteracts effect of histamine

SEX HORMONE Physiologically significant

Becomes useful during menopause in women

SYMPTOMATOLOGY

ALDOSTERONE DEFICIENCY

DECREASE IN PLASMA VOLUME LEADING TO DEHYDRATON

HYPOTENSION TO SHOCKINCREASED KMETABOLIC ACIDOSIS

SYMPTOMATOLOGY

CORTISOL DEFICIENCY

ANOREXIA, N/V, ABDOMINAL PAIN, WT LOSS, LETHARGY

HYPOGLYCEMIAHYPOTENSIONINCREASED K, WEAK PULSEPIGMENTATIONIMPAIRED STRESS TOLERANCE

SYMPTOMATOLOGY

SEX HORMONE DEFICIENCY

LOSS OF BODY HAIRLOSS OF LIBIDO OR IMPOTENCE!MENSTRUAL & FERTILITY DISORDER

ADRENAL CORTEX DISORERSADRENAL INSUFFICIENCY

ADRENAL CRISIS

CUSHING’S SYNDROME

ALDOSTERONISM

ADRENAL INSUFFICIENCY

ADDISON’S DISEASEADDISON’S DISEASEINCAPABILITY OF THE ADRENAL CORTEX TO

PRODUCE GLUCOCORTICOIDS IN RESPONSE

TO STRESS

*Hyposecretion of the adrenal cortex hormones

Assessment:

Subjective:• Muscle weakness, fatigue, lethargy, dizziness,

fainting, nausea, anorexia, abdominal pain/cramps.Objective:• V/S: decreased BP, orthostatic hypotension• Pulse: increased, collapsing, irregular• Subnormal temp.• Vomiting, diarrhea, weight loss• Tremors• Skin: poor turgor excessive pigmentation (bronze

tone)• Hyponatremia, hypoglycemia, hyperkalemia

ADRENAL CRISIS

ACUTE EPISODES FROM STRESS THAT TAXES THE ADRENAL CORTICAL FUNCTION BEYOND ITS CAPABILITIES

POSSIBLE COMPLICATION OF ADDISON’S DISEASE

ADRENAL CRISISPRECIPITATING CAUSES:ABDOMINAL DISCOMFORTINFECTIONTRAUMAHIGH TEMPEMOTIONAL UPSET

ADRENAL CRISISS/SX:

HYPOTENSIONFLUID LOSSHYPONATREMIA

ADRENAL CRISISLAB:SERUM ELEC: DECREASED Na

INCREASED KS. BUN : S. GLUCOSE: ADRENAL HORMONE ASSAY :

HYDROXYCORTICOID & 17 KETOSTEROID IN 24-HR URINE DET.

ADRENAL CRISIS

GOALS OF CARE:TO REVERSE SHOCK

RESTORE BLOOD CIRCULATION

REPLENISH NEEDED STEROID

ADRENAL CRISIS

TREATMENT:D5NSSADRENAL CORTICAL HORMONE

REPLACEMENT: INJECTABLENEOSYNEPHRINE - SHOCKHIGH SALT DIETANTIBIOTICS

CUSHING’S CUSHING’S SYNDROMESYNDROME

CAUSE:SUSTAINED OVER-PRODUCTION OF

GLUCOCORTICOIDS BY ADRENAL GLAND FROM ACTH BY PITUITARY TUMOR

EXCESSIVE GLUCORTICOID ADMINISTRATION

CUSHING’S CUSHING’S SYNDROMESYNDROMES/SX:TRUNCAL OBESITYBUFFALO HUMPMOON-FACEWT GAINSODIUM RETENTIONTHINNING OF EXTREMITIES – FROM LOSS OF

MUSCLE TISSUE DUE TO PROTEIN CATABOLISM

CUSHING’S CUSHING’S SYNDROMESYNDROME

PURPLE STRIAE – FROM THINNING OF SKINECHYMOSIS FROM SLIGHT TRAUMAANDROGENIC EFFECTS:

OLIGOMENORRHEAHIRSUTISMGYNECOMASTIA

HYPERTENSION FROM S. Na

CUSHING’S CUSHING’S SYNDROMESYNDROME

TREATMENT & NURSING CARE:

PSYCHOLOGICAL SUPPORTPREVENT INFECTION – INFLAM & IMMUNE

RESPONSE ARE SUPPRESSEDPROMOTE SAFETY SURGERY – SUB/TOTAL ADRENALECTOMY

ALDOSTERONISMALDOSTERONISMHYPERSECRETION OF ALDOSTERONE

PRIMARY – CONN’S SYNDROME

SECONDARY

CONN’S SYNDROMEPRIMARY ALDOSTERONISMCAUSE:ADRENAL ADENOMAS/SX:HYPOKALEMIAFATIGUEHYPERNATREMIA, HPN, TETANYMANAGEMENT:SURGERYALDACTONE – ALDOSTERONE ANTAGONIST

SECONDARY ALDOSTERONISMTHE PROBLEM IS OUTSIDE THE ADRENAL

GLAND:

e.g. RENIN – ANGIOTENSIN SYSTEM

ADRENAL MEDULLAHORMONES : EPINEPHRINE

NOREPINEPHRINE EFFECTS

PHEOCHROMOCYTOMATUMOR OF ADRENAL MEDULLA SECRETES INCREASED

AMOUNT OF CATECHOLAMINES

A small tumor in the adrenal gland that secretes large amounts of epinephrine and norepinephrine.

S/SX:HPNHYPERGLYCEMIACARDIAC ARRHYTHMIA & CHF DIAGNOSTIC TEST : VMA IN 24H URINE- VANILLYMANDALIC ACID

VMA IN 24H URINEEND PRODUCT OF CATECHOLAMINE

METABOLISMDRUGS & FOOD TO BE WITHHELD 24H B4 THE

TEST:COFFEE & TEABANANAVANILLACHOCOLATES

PHEOCHROMOCYTOMAMANAGEMENT:SURGERYMEDICAL : ADRENERGIC BLOCKING

AGENTS: PHENTOLAMINE

NURSING CARE:MONITOR BP IN SUPINE & STANDINGMONITOR URINE FOR GLUCOSE &

ACETONE

ANTERIOR PITUITARY ANTERIOR PITUITARY DISTURBANCESDISTURBANCES

HYPOPITUITARISM

HYPERPITUITARISM

PITUITARY ANTERIOR LOBEHORMONE HYPO FXN HYPER FXN

GH Dwarfism – young

Cachexia - adult

Gigantism – young

Acromegaly - adult

ACTH Atrophy of adrenal cortex

Cushing’s dse

TSH Atrophy & depressed thyroid fxn

Grave’s dse

FSH Atrophy & infertility Exaggerated fxn of sex organs

PROLACTIN Underdevelopment of mammary glands

Decreased milk production

MANAGEMENTHYPOPITUITARISM

SURGICAL REMOVAL / IRRADIATIONREPLACEMENT THERAPY

THYROID HORMONES STEROIDS SEX HORMONES GONADOTROPINS (restore fertility)

HYPERPITUITARISMSURGICAL REMOVAL / IRRADIATIONMONITOR FOR HYPERGLYCEMIA &

CARDIOVASCULAR PROBLEMS

POSTERIOR PITUITARY DISTURBANCES

DIABETES INSIPIDUS

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE

FUNCTION:WHEN THERE IS A OF SERUM

OSMOLALITY, THE NORMAL BODY RESPONSE IS TO THE SECRETION OF ADH.

WHEN THE NORMAL FEEDBACK MECHANISM FOR ADH IS SUSTAINED, THERE IS EXCESSIVE WATER RETENTION IN THE BODY

WHEN THERE IS OR INADEQUATE AMOUNT OF ADH, THE BODY IS UNABLE TO CONCENTRATE URINE, & EXCESSIVE H2O LOSS OCCURS

DIABETES INSIPIDUSCHARACTERIZED BY A DEFICIENCY OF CHARACTERIZED BY A DEFICIENCY OF

ADH. ADH. WHEN IT OCCURS, IT IS MOST OFTEN

ASSOCIATED WITH :NEUROLOGICAL CONDITIONS, SURGERY, TUMORS, HEAD INJURY, OR INFLAMMATORY PROBLEMS

DIABETES INSIPIDUS ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN

S/SX:POLYURIA

15-29L/ DAYPOLYDIPSIASG OF URINE IS <1.010S/SX OF DHNSHOCK

DIABETES INSIPIDUS ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN

MANAGEMENTHORMONAL REPLACEMENT – FOR LIFE

VASOPRESSIN (PITRESSIN TANNATE IN OIL) – IM OR NASAL SPRAY

NON-HORMONAL THERAPYCHLORPROPRAMIDE – INCREASE RESPONSE OF THE

BODY TO DECREASED VASOPRESSIN

INCREASE FLUIDSMONITOR I&OMAINTAIN FLUID & ELECTROLYTE BALANCE

SYNDROME OF INAPPROPRIATE ADH

(SIADH)ELEVATED ADHCAUSES:BRONCHOGENIC CANONENDOCRINE TUMORSS/SX:DECREASED SERUM SODIUM

CX IN LOC TO UNCONSCIOUSNESSSEIZURES

WATER INTOXICATIONN/VMENTAL CONFUSION

SYNDROME OF INAPPROPRIATE ADH

MANAGEMENT:WATER INTAKE RESTRICTIONADMINISTER AS ORDERED:

NaClDiureticsDemeclocycline (declamycin) – a tetracycline

analogue that interferes with the action of ADH on the collecting tubules

RECAP:ANTERIOR PITUITARY:GIANTISM, ACROMEGALLY, DWARFISM

POSTERIOR PITUITARY:DIABETES INSIPIDUS, SIADHLOCATION: BASE OF THE BRAIN

RECAPADRENAL GLAND:ADDISON’S DSECUSHING SYNDROME

ADRENAL MEDULLA:PHEOCHROMOCYTOMAPRIMARY ALDOSTERONISM

LOCATION: ON TOP OF THE KIDNEY

RECAPPANCREAS:DMLOCATION: POSTERIOR TO LIVER

PARATHYROID:HYPORATHYROIDISMHYPERPARATHYROIDISMLOCATION: NEAR THYROID

RECAPTHYROID:GOITERCRETINISMMYXEDEMAHYPERTHYROIDISM (GRAVE’S DSE)

LOCATION: ANTERIOIR PART OF NECK

QUESTION NO. 1A CLIENT IS FOUND TO BE COMATOSE &

HYPOGLYCEMIC W/ A BLOOD SUGAR OF 50 MG/DL. WHAT NURSING ACTION IS IMPLEMENTED FIRST?

A.INFUSE 1L OF D5W OVER A 12 HR PERIOD.B.ADMIN. 50% GLUCOSE IVC.CHECK THE CLIENT’S URINE FOR THE

PRESENCE OF SUGAR AND ACETONED.ENCOURAGE THE CLIENT TO DRINK ORANGE

JUICE W/ ADDED SUGAR

QUESTION NO.2WHAT IS THE PRIMARY ACTION OF INSULIN IN

THE BODY?A.ENHANCES THE TRANSPORT OF GLUCOSE

ACROSS THE CELL WALLSB.AIDS IN THE PROCESS OF GLUCONEOGENESISC.STIMULATES THE PANCREATIC BETA CELLSD.DECREASE THE INTESTINAL ABSORPTION OF

GLUCOSE

QUESTION NO.3POSTOPERATIVE THYROIDECTOMY NURSING

CARE INCLUDES WHICH MEASURES?A.HAVE CLIENT SPEAK EVERY 5-10 MINUTES IF

HOARSENESS IS PRESENTB.PROVIDE LOW-CALCIUM DIET TO PREVENT

HYPERCALCEMIAC.CHECK THE DRESSING AT THE BACK OF THE

NECK FOR BLEEDINGD.APPLY SOFT CERVICAL COLLAR TO RESTRICT

MOVEMENT

HOW TO HAVE GOOD STUDY HABITS:

Use of memory aids, mind mapping and mnemonics.Review class notes the next day. - very effective study habit - spend an hour a day reviewingCorrelate the notes and the visual aids the instructor

presentedPlan your study time when you are most receptive to

learning

Set a study goal - for 2 days I will finish endocrine

system…..GROUP STUDY - limit 4-5 person’s - group members should be mature and

serious about studying - group studying is very effective with the

exchange of ideas thru interaction but with the right mix of participants

“Only in this life, you can do good, what awaits you in the next life is not to do better, but the reward for having done your best today.”

Always remember…“…..the last few miles of

a journey are always tough, but if you keep going you’ll see that the last few steps are the most fulfilling…..”

THANK YOU…………Let us see the good, the true, and

the beautiful in life.Hope I can guide you with every step you

make, steps that we ascend the stairs of your journey to your Nursing life.

GOD BLESS