Review Endocrine Disorders FINAL
Transcript of Review Endocrine Disorders FINAL
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