Review Endocrine Disorders Final

ENDOCRINE SYSTEM 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 injury  Growth and development  Reproduction  Fluids and electrolytes  Acid base-balance  Energy metabolism

ENDOCRINE GLANDS

ENDOCRINE GLAND

HORMONES

PITUITARY TSH ANTERIOR ACTH LOBE FSH,LH

FUNCTIONS

Thyroid to release hormones Adrenal cortex to release hormones Growth, maturation & function of sex organs

Growth of body tissues & GH/ bones SOMATOTROPIN Development of PROLACTIN/ mammary glands & LTH lactation

ENDOCRINE GLANDS ENDOCRINE GLAND

HORMONE

PITUITARY POSTERIOR LOBE

ADH

Regulates water metabolism

OXYTOCIN

Stimulate uterine contractions release of milk

MSH INTERMEDIATE LOBE

FUNCTION

Affects skin pigmentation

ENDOCRINE GLANDS ENDOCRINE 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

ADRENAL MEDULLA

EPINEPHRINE NOREPINEPHRINE

FUNCTION Increase heart rate & BP Bronchodilation, Glycogenolysis Stress hormone

ENDOCRINE GLANDS ENDOCRINE GLAND

HORMONE

FUNCTION

THYROID

T3 & T4’

Regulate metabolic rate Regulate physical & mental growth & development

THYROCALCITONIN

Decrease serum Ca by increasing bone deposition

PTH PARATHYROID

Increase serum calcium by promoting bone decalcification

ENDOCRINE GLANDS ENDOCRINE GLAND

HORMONE

PANCREAS INSULIN BETA CELLS ALPHA CELLS

GLUCAGON

FUNCTION Decrease blood glucose by: Glucose diffusion across cell membrane; Converts glucose to glycogen Increase blood glucose by: Gluconeogenesis Glycogenolysis

ENDOCRINE GLANDS ENDOCRINE HORMONES GLAND OVARIES ESTROGEN & PROGESTERONE

TESTES

TESTOSTERONE

FUNCTION •Development of secondary sex

charac in female •Maturation of sex organs •Sexual functioning •Maintenance of pregnancy •Development of secondary sex

charac in male •Maturation of sex organs •Sexual functioning

HORMONE REGULATION NEGATIVE 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 TO

RELEASE 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, PR Nsg. 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, autoimmune glandular stimulation, grave’s disease - most common cause

Hyperthyroidism (cont.) DX: > elevated T3, T4 values T4= 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!!

Assessment Findings          

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

Nsg. Interventions: • Provide calm, restful envt. • physical comfort, cool envt. temp., bathe frequently w/ cool water • provide adequate rest, avoid muscle fatigue •  stressors in the envt.— noise and lights • relaxation techniques • Provide adequate nutrients •  calorie,  protein, balanced diet (4,000-5,000 cal/day) •  fluid intake • Restrict stimulants (tea, coffee, alcohol) • small, frequent feedings if hypermotility is present • Daily wt.

Nsg. Interventions: • Provide emotional support • Provide eye care • eye drops, dark glasses, patch eyes if necessary • elevate head of bed for sleep • restrict dietary sodium • assess adequacy of lid closure •Be 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 sutures check 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. Hemorrhage WOF: hypotension, tachycardia, other signs of hypovolemia WOF: irregular breathing, swelling, choking--possible hemorrhage and tracheal compression WOF: 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 neck teach 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 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)

Types •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 •Non Insulin–Dependent Diabetes Mellitus (NIDDM) or Type II  probably caused by:  disturbance in insulin reception in the cells   number of insulin receptors  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.

3.

Fasting Blood Sugar (FBS)   

NPO for 12 hours Normal value= 80-120 mg/dl 140 mg/dl or more – diagnostic of DM

Postprandial blood sugar   

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

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 Mellitus A.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 activity 2. 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 Mellitus A.Dietary Management •

• • • •

Advise use of complex carbohydrates to help stabilize blood sugar. Meal should include more fiber and starch and fewer simple or refined sugars. Avoid concentrated sweets, high in sugar (jellies, jams, cakes, ice cream) If taking insulin, eat extra food before periods of vigorous exercise Avoid periods of fasting and feasting 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. • insulin in current use may be stored at room temp., all others in ref. or cool area • avoid injecting cold insulin  lead to tissue reaction • roll insulin vial to mix, do not shake, remove air bubbles from syringe • press (do not rub) the site after injection (rubbing may alter the rate of absorption of insulin) • avoid smoking for 30 mins. after injection (cigarette smoking absorption) • Rotate sites  Failure to rotate sites may lead to Lipodystrophy  Lipodystrophy – localized disturbance of fat metabolism  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 insulin

 need : trauma, infection, fever, severe psychological or physical stress, other illnesses •  need : active exercise

Hypoglycemia  

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: •Sweating, tremor, pallor, tachycardia, palpitations and nervousness 1. caused by release of epinephrine from the CNS when blood glucose falls rapidly •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 •Give simple sugar orally if pt. is conscious and can swallow – orange juice, candy, glucose tablets, lump of sugar •Give Glucagon (SQ or IM) if pt. is unconscious or cannot take sugar by mouth •As soon as pt. regains consciousness, he should be given carbohydrate by mouth •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: 4.Hypoglycemia may be prevented by maintaining regular exercise, diet and insulin 5.Early symptoms of hypoglycemia should by recognized and treated 6.Carry at all times some form of simple carbohydrate (orange juice, sugar, candy) 7.Extra food should be taken before unusual physical activity or prolonged periods of exercise 8.Between-meal and bedtime snacks may be necessary to maintain a normal glucose level.

D-I-A-B-E-T-E-S

D- DIET: 50-60% CHO, 20-30% FATS,

10-20% CHON I- INSULIN– TYPE 1 A- ANTIDIABETIC AGENTS– TYPE 2 B- BLOOD SUGAR MONITORING E- EXERCISE T- TRANSPLANT OF PANCREAS E- ENSURE ADEQUATE FOOD INTAKE S- SCRUPULOUS FOOT CARE

Oral Antidiabetic Agents

INSULIN THERAPY DISPENSED IN “U”/ml : eg 100, 80 REFRIGERATE GIVEN @ ROOM TEMP GENTLY ROTATED, NOT SHAKEN ROUTE : SQ ; IM OR IV SYRINGE: 5/8 INCH ; SAME BRAND

INSULIN

ONSET

PEAK

DURATION

15 mins.

2-4 hrs.

6-8 hrs.

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.

Ultra rapid acting Insulin analog (Humalog) Rapid acting: Regular (Semilente)

INSULIN THERAPY: SITE OF INJECTION: ABDOMEN ANTERIOR THIGH ARM UPPER BACK BUTTOCKS

LIPODYSTROPHY CAUSE:

FAULTY TECHNIQUE TRAUMA INJECTION 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 glucose carry a rapid-acting source of glucose during exercise excessive or unplanned exercise may trigger hypoglycemia take insulin and food before active exercise

Teach pt. to practice good personal hygiene and positive health promotion to avoid diabetic complications •teach pt. about diabetic foot care •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 •help pt. identify stressful situations in lifestyle that might interfere with good diabetic control •encourage good daily hygiene •advise regular eye exams •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, thirst •nausea, vomiting, abdominal pain –-- due to acidosis •weakness, headache, fatigue --- due to acidosis and F/E imbalance •dim vision •dehydration, hypovolemic shock (PR, BP, dry skin, wt. loss) •hyperpnea (Kussmaul’s breathing) •acetone breath (fruity odor) •lethargy  COMA •Blood glucose level > 250-350 mg/100 ml.

INSULIN SHOCK LOW BLOOD SUGAR

CAUSE: OVERDOSE OF EXOGENOUS INSULIN EATING LESS OVEREXERTION WITHOUT ADDITIONAL

CALORIE INTAKE

INSULIN SHOCK S/SX: PARASYMPATHETIC HUNGER NAUSEA HYPOTENSION BRADYCARDIA

CEREBRAL LETHARGY, YAWNING SENSORIUM CX

SYMPATHETIC IRRITABILITY SWEATING TREMBLING TACHYCARDIA PALLOR

INSULIN SHOCK CLINICAL FINDING : BLOOD GLUCOSE BELOW 55-60 mg/DL TREATMENT: GLUCOSE PO ( SUGAR, ORANGE JUICE OR

CANDY) or IV ADMINISTRATION OF GLUCAGON IM, IV OR SQ

Hyperglycemic, Hyperosmolar, Non-Ketotic Coma (HHNC) • can occur when the action of insulin is severely inhibited • seen 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) lethargy temp, PR, BP, signs of severe fluid deficit Confusion, seizure, coma Blood glucose level > 600 mg/100 ml.

HHONK S/SX: S/SX OF DKA WITHOUT: KAUSMAUL’S BREATHING ACETONE BREATH METABOLIC ACIDOSIS KETONURIA

LACTIC ACIDOSIS SEVERE TISSUE ANOXIA

LACTIC ACID PRODUCTION

AGGRAVATION OF EXISTING METABOLIC 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 3.Vascular Changes •) Macroangiopathy – hardening and damage of the walls of large arteries • Coronary Artery Disease • CVA (Stroke) • Peripheral vascular disease – foot ulcers and gangrene b. ) Microangiopathy – destruction of small blood vessels • Retinopathy – damage to retinal capillaries; hemorrhage, blindness • Nephropathy – damage microcirculation of kidneys; CRF 2. Neuropathy • Damage to the neurons caused by vascular insufficiency and  blood glucose • Sensory and motor impairment • Numbness, tingling, pain in extremities • Painless neuropathy

• Impotence!!

SURPRISE!!!

PARATHYROID GLAND 4 GLANDS

SECRETES PARATHORMONE (PTH) IN RESPONSE TO SERUM Ca & Ph LEVELS

REGULATE CALCIUM & PHOSPHORUS

METABOLISM

ORGANS AFFECTED: BONES - RESORPTION KIDNEYS Ca REABSORPTION Ph EXCRETION

GIT – ENHANCES Ca ABSORPTION

Mobilization CALCIUMof calcium and STAYS IN phosphorous THE fromBONE bone

Promotes CALCIUM resorption of DEPOSITED calcium from bone maintain INtoTHE normal serum BONE calcium levels

Renal: increases EXCRETION calcium reabsorption and OF CALCIUM phosphate excretion

Hypoparathyroidism is characterized by decrease in the PTH level Promotes absorption of calcium in the GI tract ( by stimulating kidneys to convert vit.D to its active form).

HYPOCALC EMIA

•TINGLING OF FINGERS Function of calcium: •CHVOSTEKS/ maintains N muscle TROUSSEAU’S and neuromuscular •FATIGUE, WEAKNESS responses. •CARDIAC ARRHYTHMIAS Necessary component •SEIZURE for blood coagulation •BRONCHOSPASM mechanisms

HYPOPARATHYROIDISM DECREASED PTH PRODUCTION HYPOCALCEMIA CALCIUM IS: DEPOSITED IN THE BONE EXCRETED

CAUSE: HEREDITARY IDIOPATHIC SURGICAL

PARATHYROID DISORDERS DIAGNOSTIC TESTS: HEMATOLOGICAL

SERUM CALCIUM SERUM PHOSPHORUS

SERUM ALKALINE PHOSPHATASE

URINARY STUDIES URINARY CALCIUM URINARY PHOSPHATE - TUBULAR REABSORPTION OF PHOSPHATE

HYPOPARATHYROIDISM S/SX: ACUTE HYPOCALCEMIA TINGLING OF THE FINGERS CHVOSTEK’S, TROUSSEAU’S

CHRONIC HYPOCALCEMIA FATIGUE, WEAKNESS PERSONALITY CHANGES LOSS OF TOOTH ENAMEL, DRY SCALY SKIN CARDIAC ARRHYTHMIA CATARACT

HYPOPARATHYROIDISM XRAY: INCREASED BONE DENSITY MANAGEMENT: Ca SUPPLEMENT VIT D SUPPLEMENT – JUICE OR MILK, pc

LIQ FORM: WITH WATER,

SEIZURE prec

STRIDOR OR HOARSENESS TRACHEOSTOMY SET @ BEDSIDE CaGLUCONATE @ BEDSIDE  LISTEN FOR

CALCIUM of Mobilization RELEASED INTO calcium and THE BLOOD phosphorous LEADS TO BONE from bone DAMAGE

HYPERCALCEMIA, Promotes LACK OF RESORPTION resorption of OF CALCIUM INTO THE calcium from BONE( BONE CYST bone to maintain AND PATHOLOGIC normal serum FRACTURE) calcium levels

TUBULAR CALCIUM Renal: increases DEPOSITKIDNEY calcium STONES, AZOTEMIA, reabsorption and HPN BY RF, RENAL phosphate FAILURE

excretion

Hyperparathyroidism is characterized by excesssive secretion of PTH

Promotes absorption of ANOREXIA calcium in the GI tract N/V kidneys ( by stimulating CONSTIPATION to convert vit.D to its active form). PEPTIC ULCER DSE

Function of calcium: MUSCLE  maintains N muscle WEAKNESS and neuromuscular responses. PERSONALITY Necessary component CHANGES for blood coagulation CARDIAC mechanisms

ARRHYTHMIAS

HYPERPARATHYROIDISM INCREASED PTH PRODUCTION HYPERCALCEMIA HYPOPHOSPHATEMIA

PRIMARY –

TUMOR OR HYPERPLASIA OF THE PARATHYROID GLAND

SECONDARY –

COMPENSATORY OVERSECRETION OF PTH IN RESPONSE TO HYPOCALCEMIA FROM:  CHRONIC RENAL DSE  RICKETS  MALABSORPTION SYNDROME  OSTEOMALACIA

HYPERPARATHYROIDISM S/SX: BONE PAIN : ESP @ THE BACK, PATHOLOGIC

FRACTURES TUBULAR CALCIUM DEPOSITS - KIDNEY STONES, RENAL COLIC, POLYURIA, POLYDIPSIA MUSCLE WEAKNESS PERSONALITY CX, DEPRESSION CARDIAC ARRHYTHMIAS, HPN

XRAY: BONE DEMINERALIZATION

HYPERPARATHYROIDISM MANAGEMENT:

TX OF CHOICE : SURGICAL REMOVAL OF HYERPLASTIC TISSUE

IV PNSS 5L/ DAY WITH DIURETICS CRANBERRY JUICE (ACID-ASH) LOW Ca, HIGH Ph DIET NO MILK, CAULIFLOWER & MOLASSES

FOR STONES CARE FOR PARATHYROIDECTOMY STRAIN URINE

ADRENAL GLAND STIMULATED BY ACTH ADRENAL MEDULLA- SECRETES

CATECOLAMINE, EPINEPHRINE, & NOREPINEPHRINE. ADRENAL CORTEX- MAIN BODY; RESP FOR SECRETION OF GLUCO,MINERALO, SEX HORMONES (ANDRO & ESTRO) FUNCTION IS TO CONTROL THE (-) FEEDBACK MECHANISMS REGULATING HORMONE RELEASE

ADRENAL GLAND HORMONE ALDOSTERONE

FUNCTION

Renal : Na & Cl reabsorption; K excretion GI : Na absorption • increase serum glucose by GLUCOCORTICOIDS 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 SHOCK INCREASED K METABOLIC ACIDOSIS

SYMPTOMATOLOGY CORTISOL DEFICIENCY ANOREXIA, N/V, ABDOMINAL PAIN, WT LOSS,

LETHARGY HYPOGLYCEMIA HYPOTENSION INCREASED K, WEAK PULSE PIGMENTATION IMPAIRED STRESS TOLERANCE

SYMPTOMATOLOGY SEX HORMONE DEFICIENCY LOSS OF BODY HAIR LOSS OF LIBIDO OR IMPOTENCE! MENSTRUAL & FERTILITY DISORDER

ADRENAL CORTEX DISORERS ADRENAL INSUFFICIENCY ADRENAL CRISIS CUSHING’S SYNDROME ALDOSTERONISM

ADRENAL INSUFFICIENCY

ADDISON’S DISEASE INCAPABILITY 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

DISEASE

ADDISON’S

ADRENAL CRISIS PRECIPITATING CAUSES: ABDOMINAL DISCOMFORT INFECTION TRAUMA HIGH TEMP EMOTIONAL UPSET

ADRENAL CRISIS S/SX: HYPOTENSION FLUID LOSS HYPONATREMIA

ADRENAL CRISIS LAB: SERUM ELEC: DECREASED Na INCREASED K S. 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: D5NSS ADRENAL CORTICAL HORMONE

REPLACEMENT: INJECTABLE NEOSYNEPHRINE - SHOCK HIGH SALT DIET ANTIBIOTICS

CUSHING’S SYNDROME CAUSE: SUSTAINED OVER-PRODUCTION OF GLUCOCORTICOIDS BY ADRENAL GLAND FROM

ACTH BY PITUITARY TUMOR EXCESSIVE GLUCORTICOID

ADMINISTRATION

CUSHING’S SYNDROME S/SX:

TRUNCAL OBESITY BUFFALO HUMP MOON-FACE WT GAIN SODIUM RETENTION THINNING OF EXTREMITIES – FROM LOSS OF MUSCLE TISSUE DUE TO PROTEIN CATABOLISM

CUSHING’S SYNDROME PURPLE STRIAE – FROM THINNING OF SKIN ECHYMOSIS FROM SLIGHT TRAUMA ANDROGENIC EFFECTS: OLIGOMENORRHEA HIRSUTISM GYNECOMASTIA HYPERTENSION FROM S. Na

CUSHING’S SYNDROME TREATMENT & NURSING CARE: PSYCHOLOGICAL SUPPORT PREVENT INFECTION – INFLAM & IMMUNE RESPONSE ARE SUPPRESSED PROMOTE SAFETY SURGERY – SUB/TOTAL ADRENALECTOMY

ALDOSTERONISM HYPERSECRETION OF ALDOSTERONE

PRIMARY – CONN’S SYNDROME SECONDARY

CONN’S SYNDROME PRIMARY ALDOSTERONISM CAUSE: ADRENAL ADENOMA

S/SX:

HYPOKALEMIA FATIGUE HYPERNATREMIA, HPN, TETANY

MANAGEMENT:

SURGERY ALDACTONE – ALDOSTERONE ANTAGONIST

SECONDARY ALDOSTERONISM THE PROBLEM IS OUTSIDE THE ADRENAL

GLAND:

e.g. RENIN – ANGIOTENSIN SYSTEM

ADRENAL MEDULLA HORMONES : EPINEPHRINE NOREPINEPHRINE EFFECTS

PHEOCHROMOCYTOMA  TUMOR 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: HPN HYPERGLYCEMIA CARDIAC ARRHYTHMIA & CHF DIAGNOSTIC TEST : VMA IN 24H URINE- VANILLYMANDALIC

ACID

VMA IN 24H URINE END PRODUCT OF CATECHOLAMINE

METABOLISM

DRUGS & FOOD TO BE WITHHELD 24H B4 THE

TEST:

COFFEE & TEA BANANA VANILLA CHOCOLATES

PHEOCHROMOCYTOMA MANAGEMENT: SURGERY MEDICAL : ADRENERGIC BLOCKING

AGENTS: PHENTOLAMINE

NURSING CARE: MONITOR BP IN SUPINE & STANDING MONITOR URINE FOR GLUCOSE &

ACETONE

ANTERIOR PITUITARY DISTURBANCES HYPOPITUITARISM HYPERPITUITARISM

PITUITARY ANTERIOR LOBE HORMONE

HYPO FXN

GH

Dwarfism – young Cachexia - adult Atrophy of adrenal cortex

Gigantism – young Acromegaly - adult Cushing’s dse

Atrophy & depressed thyroid fxn Atrophy & infertility

Grave’s dse

ACTH TSH FSH PROLACTIN

Underdevelopment of mammary glands

HYPER FXN

Exaggerated fxn of sex organs Decreased milk production

MANAGEMENT HYPOPITUITARISM SURGICAL REMOVAL / IRRADIATION REPLACEMENT THERAPY  THYROID HORMONES  STEROIDS  SEX HORMONES  GONADOTROPINS (restore fertility)

HYPERPITUITARISM SURGICAL REMOVAL / IRRADIATION MONITOR 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 INSIPIDUS CHARACTERIZED BY A DEFICIENCY OF ADH. WHEN IT OCCURS, IT IS MOST OFTEN ASSOCIATED WITH : NEUROLOGICAL CONDITIONS, SURGERY, TUMORS, HEAD INJURY, OR INFLAMMATORY PROBLEMS

DIABETES INSIPIDUS / PARTIAL DEFICIENCY OF VASOPRESSIN

S/SX: POLYURIA 15-29L/ DAY POLYDIPSIA SG OF URINE IS <1.010 S/SX OF DHN SHOCK

ABSOLUTE

DIABETES INSIPIDUS

ABSOLUTE / PARTIAL DEFICIENCY OF VASOPRESSIN

MANAGEMENT HORMONAL REPLACEMENT – FOR LIFE  VASOPRESSIN (PITRESSIN TANNATE IN OIL)

OR NASAL SPRAY

NON-HORMONAL THERAPY  CHLORPROPRAMIDE

– INCREASE RESPONSE OF THE

BODY TO DECREASED VASOPRESSIN

INCREASE FLUIDS MONITOR I&O MAINTAIN FLUID & ELECTROLYTE

BALANCE

– IM

SYNDROME OF INAPPROPRIATE ADH (SIADH) ELEVATED ADH

CAUSES: BRONCHOGENIC CA NONENDOCRINE TUMORS S/SX: DECREASED SERUM SODIUM

 CX IN LOC TO UNCONSCIOUSNESS  SEIZURES

WATER INTOXICATION  N/V

 MENTAL CONFUSION

SYNDROME OF INAPPROPRIATE ADH MANAGEMENT: WATER INTAKE RESTRICTION ADMINISTER AS ORDERED: NaCl Diuretics Demeclocycline (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, SIADH

LOCATION: BASE OF THE BRAIN

RECAP ADRENAL GLAND: ADDISON’S DSE CUSHING SYNDROME ADRENAL MEDULLA: PHEOCHROMOCYTOMA PRIMARY ALDOSTERONISM

LOCATION: ON TOP OF THE KIDNEY

RECAP PANCREAS: DM

LOCATION: POSTERIOR TO LIVER PARATHYROID: HYPORATHYROIDISM HYPERPARATHYROIDISM

LOCATION: NEAR THYROID

RECAP THYROID: GOITER CRETINISM MYXEDEMA HYPERTHYROIDISM (GRAVE’S DSE)

LOCATION: ANTERIOIR PART OF NECK

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

HYPOGLYCEMIC W/ A BLOOD SUGAR OF 50 MG/DL. WHAT NURSING ACTION IS IMPLEMENTED FIRST? B.INFUSE 1L OF D5W OVER A 12 HR PERIOD. C.ADMIN. 50% GLUCOSE IV D.CHECK THE CLIENT’S URINE FOR THE PRESENCE OF SUGAR AND ACETONE E.ENCOURAGE THE CLIENT TO DRINK ORANGE JUICE W/ ADDED SUGAR

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

IN THE BODY? B.ENHANCES THE TRANSPORT OF GLUCOSE ACROSS THE CELL WALLS C.AIDS IN THE PROCESS OF GLUCONEOGENESIS D.STIMULATES THE PANCREATIC BETA CELLS E.DECREASE THE INTESTINAL ABSORPTION OF GLUCOSE

QUESTION NO.3 POSTOPERATIVE THYROIDECTOMY NURSING

CARE INCLUDES WHICH MEASURES? B.HAVE CLIENT SPEAK EVERY 5-10 MINUTES IF HOARSENESS IS PRESENT C.PROVIDE LOW-CALCIUM DIET TO PREVENT HYPERCALCEMIA D.CHECK THE DRESSING AT THE BACK OF THE NECK FOR BLEEDING E.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 reviewing Correlate the notes and the visual aids the instructor presented Plan 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