KMB II SISTEM ENDOKRIN

Chrisnawati, BSN, MSN

21 Maret 2022
08:00 s.d 12:00 WITA
 Tren dan Isu
Gangguan Sistem Endokrin di Indonesia
 Termasuk dalam kategori PTM (penyakit tidak menular), penyebab utama kematian secara
global
 Kasus yang paling sering ditemukan: DM tipe 2, Obesitas, Osteoporosis, dislipidemia,
hipertiroidisme, hipotiroidisme, dan sindrom Cushing.
 Penyebab: Gaya hidup tidak sehat
 Pemeriksaan Diagnostik
 Pemeriksaan Secara Umum
 Pemeriksaan Laboratorium
 Pemeriksaan untuk masing-masing organ
Pemeriksaan Secara Umum:

 Pengumpulan urine selama 24 jam

 Test Stimulasi ACTH
 Test kepadatan tulang
 Test stimulasi hormone Pelepas CRH
 Test Supresif deksametason
 Test toleransi glukosa oral
 Test Tiroid
 USG
 Endoscopic ultrasound
 CT Scan
 MRI (Magnetic Resonance Imaging
 Pengambilan darah vena
 Tes darah hormone perangsang tiroid
Pemeriksaan Laboratorium

 Pemeriksaan urine
 Pemeriksaan Darah
Pemeriksaan untuk masing-masing organ
 Pemeriksaan pada kelenjar Hipofisis: foto tengkorak, foto tulang, dan CT scan otak,
pemeriksaan kadar hormone: GH, TSH, ACTH
 Pemeriksaan kelenjar tiroid: uptake radioaktif, Tes T3 dan T4 serum, uptake resin, protein
bound iodine, laju metabolism basal dan scanning tiroid
 Pemeriksaan kelenjar paratiroid: percobaan Sulkowitch, percobaan Ellwort-Howard,
Percobaan Kalsium Intravena
 Pemeriksaan kelenjar Pankreas: Gula darah puasa dan 2 jam setelah makan (2 jam PP)
 Pemeriksaan kelenjar adrenal: pemeriksaan hemokonsentrasi darah, pemeriksaan elektrolit
serum, percobaan vanil Mandelic Acid (VMA) dan tes stimulasi
 Pemeriksaan lain: pemeriksaan radiologi, pemeriksaan EKG, pemeriksaan EMG
(elektromiogram)
 ASUHAN KEPERAWATAN PADA KLIEN
DENGAN MASALAH KELENJAR HIPOFISIS
Hormon Hipofisis
 DIABETES INSIPIDUS
 PATHOPHYSIOLOGY & ETIOLOGY
1. A deficient production of secretion of the ADH by the posterior pituitary
gland decreasing reabsorption of water in nephron tubules.
2. May be familial, idiopathic, secondary to trauma, surgery tumors,
infections or autoimmune disorders.
3. Neurogenic diabetes insipidus, a renal tubular defect resulting in decreased
water absorption results in impaired renal concentrating ability
Clinical Finding
 Subjective: Polydipsia, craving for cold water
 Objective:
1. Polyuria (5 to 24 L/24 hour)
2. Dilute Urine, specific gravity 1.001 to 1.005; osmolality 50 to 200 mOsm/kg
3. Increased serum sodium and plasma osmolality
4. Signs of dehydration (poor skin turgor, dry mucous membranes, elevated temperature)
 Therapeutic Intervention
 Antidiuretic hormone replacement, vasopressin
 Treatment of underlying cause
 Hypophysectomy
 NURSING CARE OF CLIENTS WITH
DIABETES INSIPIDUS
A. ASSESSMENT
A. Intake and output, weight and specific gravity of urine to establish baseline data
B. Results of serum electrolyte evaluation
C. Dryness of skin and mucous membranes
B. NURSING DIAGNOSES
A. Deficient fluid volume related to polyuria
B. Ineffective therapeutic regimen management related to chronicity of problem
 NURSING CARE OF CLIENTS WITH DIABETES INSIPIDUS
 Planning/Implementation
1. Monitor fluid and electrolyte status; intake and output, daily weight, skin turgor, electrolyte
levels
2. Replace fluid by mouth or parenterally
3. Monitor response to ADH replacement
4. Teach client on long term vasopressintherapy the need for daily weight records, recognition of
polyuria, and wearing a medical alert bracelet, overdosage may cause syndrome of inappropriate
antidiuretic hormone (SIADH), leading to water retention and hyponatremia
5. Advise client to advoid alcohol because it suppresses ADH secretion
 Evaluation/outcomes
1. Maintain fluid balance
2. States signs of overmedication and undermedication with ADH replacement
 SIADH (Syndrome of Inappropriate
antidiuretic hormone secretion)
 PATHOPHYSIOLOGY & ETIOLOGY
1. Excessive ADH Secretion leads to fluid retention and dilutional
hyponatremia
2. May be caused by head trauma, tumors, or infections, malignant
tumor cells may produce ADH
CLINICAL FINDING

1. Subjective: Anorexia, nausea, fatique, headache

2. Objective:
a. Reduced urine output
b. Decreased deep tendon reflexes
c. Change in mental status, seizures, coma
d. Signs of fluid retention such as weight gain, crackles, jugular vein distention
e. Decrease serum sodium and osmolality
3. Therapeutic Interventions: fluid restriction, hypertonic parenteral fluids
Nursing care of Clients with Syndrome of Inappropriate
Antidiuretic Hormone Secretion (SIADH)

 ASSESSMENT
1. History of maliginancy, infection or increased intracranial pressure
2. Intake and output, daily weight, vital signs
3. Serum and urine for sodium and osmolality
4. Neurologic evaluations
 NURSING DIAGNOSES
1. Excess fluid volume related to fluid retention
2. Risk for injury related to altered neurologic function
 PLANNING/IMPLEMENTATION
 EVALUATION/OUTCOMES
Nursing care of Clients with Syndrome of Inappropriate
Antidiuretic Hormone Secretion (SIADH)

 PLANNING/IMPLEMENTATION
1. Monitor fluid and electrolyte status
2. Restrict fluid intake, administer hypertonic intravenous solutions as ordered
3. Institute seizure precautions
4. Provide supportive measures for related disorders
 EVALUATION/OUTCOMES
1. Maintain fluid balance
2. Remains seizure free
ASUHAN KEPERAWATAN PADA KLIEN
DENGAN MASALAH KELENJAR TIROID
 HIPERTIROID
 PATHOPHYSIOLOGY & ETIOLOGY
1. Excessive concentration of thyroid hormones in the blood as a result of
thyroid disease or increased TSH, Leads to a hypermetabolic state
2. Etiology of Grave’s disease is mediated by immunoglobulin G (IgG)
antibody that actives TSH receptors on the surface of Thyroid cells.
3. Etiology of Grave’s disease is believed to be involved with an autoimmune
process of impaired regulation, associated with to other autoimmune
disorders
4. The gland may also enlarge (goiter)as a result of decreased iodine intake, no
increase in secretion of thyroid is present
CLINICAL FINDING
1. Subjective: Polyphagia, emotional lability, apprehension, heat intolerance
2. Objective:
a. Weight loss, loose stools, tremors, hyperactive reflexes, diaphoresis, insomnia, exophthalmos,
corneal ulceration, increased systolic blood pressure,temperature, pulse and respiration.
b. Decreased TSH Level if thyroid disorder, increased TSH Level if secondary to a pituitary
disorder
c. Graves’ disease generally involves hyperthyroidism, goiter, and exophthalmos
d. Increased triiodothyronine (T3), Thyroxine (T4), protein bound iodine (PBI), long acting thyroid
stimulator (LATS), and radioactive iodine uptake
e. Thyrotoxic crisis (thyroid storm): a state of hypermetabolism that may lead to heart failure,
usually precipitated by a period of severe physiologic or psychologic stress, thyroid surgery, or
radioactive iodine therapy
Therapeutic Interventions

1. Antithyroid medication to block the synthesis of thyroid hormone

2. Antithyroid medication such as iodine (potassium iodine) to reduce the vascularity of the
thyroid gland
3. Radioactive iodine to destroy thyroid gland cell, thereby decreasing the production of the
thyroid hormon
4. Medication to relieve symptoms related to the increased metabolic rate such as adrenergic
blocking agents
5. Well balanced, high calorie diet with vitamin and mineral supplements
6. Surgical intervention involves a subtotal or total thyroidectomy
 Nursing care of Clients with Hyperthyroidism
 ASSESSMENT
1. History of weight loss, diarrhea, insomnia, emotional lability, palpitations, and heat intolerance
2. Eyes for exophthalmos, tearing, and sensitivity to light
3. Neck palpitation for enlarged thyroid gland
4. Weight and vital signs to establish baseline
 NURSING DIAGNOSES
1. Ineffective coping related to emotional lability
2. Imbalanced nutrition: less than body requirements related to increased metabolic needs
Nursing care of Clients with Hyperthyroidism

 PLANNING/IMPLEMENTATION
1. Use measures such as decreased stimulation medications, and back rub to establish a climate for
uninterrupted rest
2. Keep the room cool
3. Provide diet high in calories, protein and carbohydrates with supplemental feeding between
melas and at bedtime, vitamin and mineral supplements should be given as prescribed
4. Understand that the clients is upset by lability of mood and exaggrerated response to
environmental stimuli: take time to explain disease processes involved
5. Provide eye drops or pathes as needed
Nursing care of Clients with Hyperthyroidism
 Care for the client before a thyroidectomy
1. Administer prescribed antithyroid medications to achiever euthyroid state
2. Teach deep breathing exercise and use of hands to support neck and to avoid strain on suture line
 Care for the client following a thyroidectomy
1. Observe for signs of respiratory distress and laryngeal stridor caused by tracheal edema
2. Provide humidity with cold steam nebulizer to keep secretions moist when at home
3. Keep the bed in a semi fowler’s position
4. Observe dressings at the operative site and back of the neck and shoulders for signs of
hemorrhage
Nursing care of Clients with Hyperthyroidism
 Care for the client following a thyroidectomy
1. Observe for signs of thyroid storm such as high fever, tachycardia, irritability, delirium, coma, may result
from manipulation of the gland during surgery, which release thyroid hormone into bloodstream
2. Notify physician immediately if signs of thyroid storm occur
3. Observe for signs of tetany such as numbness or twitching of extremities, spasm of the glottis,
hypocalcemia can occur after accidental trauma or removal the parathyroid glands
4. Assess for hoareness; may result from endotracheal intubation or laryngel nerve damage
 Nursing care of Clients with Hyperthyroidism
 Provide teaching regarding radioactive iodine therapy

1. Following therapy client returns to the community

2. Hospitalization in isolation may be required for several days if larger doses are used
3. Symptoms of hyperthyroidism may take 3 to 4 weeks to subside

 Teach client signs and symptoms of:

1. Hypothyroidism as a result of treatment
2. Hypothyroidism as a result of thyroid storm or overmedication with thyroid hormone replacement therapy
 Teach the importance of taking antithyroid medications regularly an to observe adverse effects

 EVALUATION/OUTCOMES
1. Maintain ideal body weight
2. Establishes regular routine of activity and rest
 HIPOTIROID
 Pathophysiology and Etiology
1. Congenital thyroid defect
2. Defective hormone synthesis
3. Prenatal and postnatal iodine deficiency
4. Therapy for hyperthyroidism, thyroid medication, thyroid surgery, radioactive iodine
5. Autoimmune disease such as Hashimoto’s disease and sarcoidosis
6. Classified according to the time of life in which occurs
a. Cretinism: hypothyroidism found at birth
b. Lymphocytic thyroiditis most frequently appears after 6 years of age and peaks during adolescence,
generally self limiting
c. Hypothyroidism without myxedema, mild degree of thyroid failure in older children and adults
d. Hypothyroidism with myxedema, severe degree of thyroid failure in older individuals
Pathophysiology and Etiology
 Decreased level of thyroid hormone (T3 and T4) slows the basal metabolic rate (BMR), the
decreased BMR affects lipid metabolism, increased cholesterol and triglyceride levels and
affects RBC production leading to anemiaand folate deficiency.
 Myxedema coma is the most severe degree of hypothyroidism, representing a
potentiallyfatal endocrine emergency, precipitated by a severe physiologic stress,
myxedema coma involves hypothermia, bradycardia, hypoventilation, and progressive loss
of conciousness
CLINICAL FINDING
1. Subjective: dull mental processes, apathy, lethargy, loss of libido, intolerance to cold,
anorexia
2. Objective:
a. Lack of facial expression, increase in weight, constipation, subnormal temperature and pulse, dry,
brittle hair and nails, pale, dry, coarse skin, enlarge tongue, drooling, hoarseness, thinning of
lateral eyebrows, scalp, axilla, and pubic hair loss, diminished hearing, anemia, periorbital
anemia
b. Decreased basal metabolic rate (BMR)
c. Decreased thyroxine (T4), Triiodothyronine (T3), and radioactive iodine uptake, delayed or poor
response to TSH stimulation test in secondary hypothyroidism, increased TSH in primary
hypothyroidism
 Therapeutic Intervention:
Administer thyroid hormones, maintain vital functions
Nursing care of Clients with Hypothyroidism

 ASSESSMENT
1. History that may have contributed to condition
2. Activity tolerance, bowel elimination, sleeping patterns, sexual function, and intolerance to cold
3. Skin and hair for characteristic changes
4. Weight and vital signs to establish baseline
5. Signs of anemia, atherosclerosis, or arthritis
 NURSING DIAGNOSES
1. Activity intolerance related to decreased metabolic rate
2. Constipation related to decreased gastrointestinal activity
Nursing care of Clients with Hypothyroidism

 Planning/Implementation
1. Have patience with lethargic client, activity tolerance and mental functioning will improve with
therapy
2. Teach the client and family to be alert for signs of complications
a. Angina pectoris: chest pain, indigestion
b. Cardiac Failure: dyspnea, palpitations
c. Myxedema coma: weakness, syncope, slow pulse rate, subnormal temperature, slow respirations,
lethargy

3. Teach the client to seek medical supervision regularly and when signs of illness develop
4. Explain the importance of continued hormone replacement throughout life
 Nursing care of Clients with Hypothyroidism

 Planning/Implementation
5. Review the signs of hypothyroidism and hyperthyroidism to help client recognize signs of
undermedication or overmedication
6. Explain that increased sensitivity to narcotic analgesics and tranquilizers necessitates dosage adjustment;
OTC drugs should be avoided unless approved by physician
7. Help the client and family recognize that client’s inability to adapt to cold temperature requires additional
protection and modification of outdoor activity in cold weather
8. Teach the client to avoid constipation by the use of adequate hydration and roughate in the diet
9. Apply moisturizers to skin
10. Teach the need to restrict calories, cholesterol, and fat in the diet
 Evaluation/outcome
1. Completes activity of daily living (ADL) without fatigue
2. Complies with dietary exercise, and medication regimen
3. Establishes regular pattern of bowel elimination
KANKER TIROID
 ASSESSMENT
 NURSING DIAGNOSES
 PLANNING/IMPLEMENTATION
 EVALUATION/OUTCOMES
TIROIDITIS
 ASUHAN KEPERAWATAN PADA KLIEN
DENGAN MASALAH KELENJAR PANKREAS
(PULAU LANGERHANS)
 DIABETES MELLITUS
Data Base
 ETIOLOGY & PATHOPHYSIOLOGY
1. Hyperglycemia occurs when there is insufficient secretion of insulin, cells become insulin resistant,
and/or hepatic glucose production is increased
2. Body attempts to rid itself of excess glucose by excreting some via kidneys; an osmotic force is
created within the kidneys; an osmotic force is created within the kidneys because of the glucose
excretion and body fluid is lost
3. If the body unable to use carbohydrates for cellular function fat is oxidized as a compensatory
mechanism, oxidation of fats gives of keton bodies
4. Risk factors
1. Type1: genetic predispotion; environmental factors such as toxins or viruses, age < 30 years
2. Type2: family history; obesity, usually age ≥45 years, history of gestational diabetes, increasing incidence
in childhood and adolescence
 DIABETES MELLITUS
 Classification
a. Type 1: formerly known as insulin dependent diabetes mellitus (IDDM); destruction of
beta cells leads to an inability to produce insulin; requires exogenous insulin
b. Type 2: formerly known as non-insulin dependent diabetes mellitus (NIDDM); has a
gradual onset and the pancreas produces some insulin so that ketoacidosis is not likely ;
may be controlled with adherence to a diet and exercise program that promotes
maintenance of a desirable weight; account for 90% of diabetes
c. Gestational: detected during 24 to 28 weeks’ gestation; glucose levels are generally normal
6 weeks postpartum; more likely to develop type 2 diabetes 5 to 10 years after delivery;
neonate exhibits macrosomia, hypoglycemia, hypocalcemia, and hyperbilirubinemia
d. Diabetes mellitus associated with other conditions or syndromes (formerly known as
secondary diabetes); associated with conditions such as cushing’s disease, pancreatic
disease, and glucocorticoid medication
e. Impaired glucose tolerance; high glucose levels but not sufficiently high to be diagnostic
for diabetes
 DIABETES MELLITUS
 Acute increase in serum glucose levels; diabetic ketoacidosis (DKA) and Hyperglycemic
Hyperosmolar nonketotic syndrome (HHKS)
a. Cause: insufficient insulin, major stresses (e.g., infection, surgery, trauma, pregnancy,
emotional turmoil, nausea and vomiting), or drugs (Steroids)
b. Pathophysiology
1) DKA is associated with type 1; with inadequate insulin to support basal needs, proteins and fats
are used; ketones are excreted via urine and breating; dehydration and electrolyte imbalance
occur
2) HHKS is associated with type 2; hyperglycemia increases intravascular osmotic pressure, leading
to polyuria and cellular dehydration
 DIABETES MELLITUS
 Acute decrease in serum glucose: insulin shock or reaction
a. Causes: excess insulin or oral antidiabetic medications; too little food or too much exercise
when receiving antidiabetic medications
b. Pathophysiology: excessive insulin lowers serum glucose as glucose is carried into cells;
decreased food intake in relation to prescribed antidiabetic medications results in
hypoglycemia; excessive exercise uses glucose for metabolism decreasing serum glucose
 Long Term complications of diabetes include microangiopathy (retinopathy, nephropathy),
macroangiopathy (peripheral vascular disease, arterioatheroscelrosis, coronary artery
disease, cerebral vascular disease), neuropathy, skin problems (cellulitis, fungal infections,
boils), periodontal disease
 Clinical Findings
1) Subjective: polydipsia; polyphagia, fatigue; blurred vision (retionopathy, osmotic changes);
peripheral neuropathy
2) Objective:
a. Polyuria: weight loss; glucosuria; peripheral vascular changes; ulcers; gangrene
b. Hyperglycemia: detected by fasting blood sugar, glucose tolerance test, 2 hour post prandial glucose,
and glycosylated hemoglobin or hemoglobin A1c (provides measure of average glucose level over
preceding 2 to 3 months)
 DKA and HHKS
a. Hyperglycemia, glycosuria, polyuria
b. Dehydration: flushed, hot, dry skin, decreased skin turgor (tenting), hypotension, tachycardia, thirst,
headache, confusion, drowsiness
c. Metabolic acidosis (DKA only): Kussmaul respirations as body attempts to blow off carbo dioxide;
ketonuria, sweet breath odor, anorexia, nausea, vomiting, decreased serum pH, decreased PCO2
 Clinical Findings
 Hypoglycemia (insulin shock or reaction)
a. Occurs as a result of sympathetic nervous stimulation or reduced cerebral glucose supply
b. CNS effects: mental confusion, blurred vision, diplopoa, slurred speech, fatigue, seizures
c. SNS (adrenergic) effects: nervousness, weakness, pallor, diaphoresis, tremor, tachycardia,
hunger
 THERAPEUTIC INTERVENTIONS
a. Lifestyle changes
 Weight control: obesity leads to insulin resistance; this can be reversed by weight loss
 Exercise: increase insulin sensitivity but must be regular; brisk walking, swimming, and bicycling are
recommended
 Diet: current recommendations include:
1) Caloric control to maintain ideal body weight
2) 50% to 60% of caloric intake should be from carbohydrates, high-fiber foods rich in water-soluable fiber (oat
bran, peas, all forms of beans, pectin-rich fruits and vegetables); food with a high glycemic index should be
avoided; glycemic index refers to effect of particular foods on blood glucose
3) Protein: intake should be consistent with the dietary guidelines, usually between 60 and 85 gr; should be 12% to
20% of daily calories
4) Fat intake not to exceed 30% of daily calories (70 to 90 g/day); keep saturated fat intake low; emphasized mono-
and polyunsaturated fats
5) Dietary ratio: carbohydrate to protein to fat usually about 5:12
6) Distribute food fairly evenly throughout the day in three or four meals, with snacks added between and at
bedtime as needed in accordance with total food allowance and therapy (insulin or oral hypoglycemics)
7) Basic tools for planning diet: Diabetes Food Guide Pyramid, food composition tables showing nutrient content
and glycemic index of foods

b. Self monitoring of blood glucose (SMBG)

 THERAPEUTIC INTERVENTIONS
1) Adjusted after considering the client’s physical and emotional stresses; a specific type of
insulin and schedule is prescribed
2) Somogyi effect: insulin-induced hypoglycemia rebounds to hyperglycemia
 Epinephrine and glucagon are released in response to hypoglycemia
 These reactions cause mobilization of the liver’s stored glucose and iatrogenically induce
hyperglycemia
 Somogyi phenomenon is treated by gradually lowering insulin dosage while monitoring blood
glucose, particularly during the night (when hypoglycemia is most likely to occur)
 Must be differentiated from the dawn phenomenon, early morning hyperglycemia attributed to
increased secretion of growth hormone, this requires delaying administration of pm insulin and
increased dosage
 THERAPEUTIC INTERVENTIONS
 Insulin pump
1. External battery operated device that delivers insulin through a needle inserted into
subcutaneous tissue
2. Small (basal) doses of regular insulin are programmed into computer to be delivered every
few minutes, bolus doses (extra preset amounts) are delivered before meals
3. Improves glucose control for clients with wide variations in insulin need as a result of
irregular schedules, pregnancy, or growth requirements
4. A prescribed amount of insulin for 24 hours plus priming is drawn into syringe
5. The administration set is primed and needle inserted aseptically, usually into subcutaneous
tissue of abdomen
 THERAPEUTIC INTERVENTIONS
 Oral antidiabetics for certain clients with type 2 diabetes who cannot be managed with
lifestyle change alone; must have some functioning beta cells in the islet of Langerhans
 Other therapies include pancreatic islet cell grafts, pancreas transplants, implantable
insulin pumps that continually monitor blood glucose and release insulin accordingly,
cyclosporin therapy to prevent beta cell destruction in type 1 diabetes
 THERAPEUTIC INTERVENTIONS
 Management of DKA and HHKS
a. IV to provide fluid replacement and direct access to the circulatory system, and a foley
catheter to monitor urine output
b. Rapid-acting insulin based on serum glucose levels
c. Replacement of lost electrolytes, particularly sodium and potassium, using blood studies to
determine dosage, when insulin is administered potassium reenters the cell resulting in
hypokalemia
d. Cardiac monitoring if circulatory collapse is imminent or dysrhythmias associated with
electrolyte imbalance occur
e. Treat acidosis according to cause
 THERAPEUTIC INTERVENTIONS
 Management of hypoglycemia (insulin shock or reaction)
a. 10 to 15 g of simple sugar (e.g., glucose tablets, 4 to 6 ounces of juice or soda, hard candy)
followed by complex carbohydrate and protein (e.g., cheese and crackers)
b. Establish an intervenous line for circulatory access
c. Administration of 50% dextrose solution
d. If unconscious, glucagon injection to stimulate glycogenolysis
 Nursing Care of Client with Diabetes Mellitus

A. ASSESSMENT
1. Familial history of diabetes mellitus
2. Cardinal signs of polyuria, polydipsia, an polyphagia
3. History of fatigue, visual changes, impaired wound healing, urinary tract infections, fungal
infections, and altered sensation
4. Blood glucose levels, hemoglobin A1c
5. Visual acuity and retinal changes
6. Vital signs and weight for baseline data
7. Urine for acetone, microalbumin
8. Renal Function
9. Dietary and exercise
 ANALYSIS/NURSING DIAGNOSES

1. Ineffective therapeutic regimen management related to complexity of therapies and

chronicity of the illness
2. Imbalanced nutrition: less than body requiredments related to impaired carbohydrate, fat,
and protein metabolism
 PLANNING/IMPLEMENTATION
1. Assist the client and family to understand the disease process
2. Encounterage the client to express feelings about illness and the necessary changes in
lifestyles and self image
3. Help the client with the administration of medication until self-administration is both
physically and psychologically possible
4. Assist the client in recognizing the need for activities and diet that promote and maintain
normal body weight
5. Monitor serum glucose with routine finger sticks
6. Test urine for ketones when glucose is high, obtain double voided specimen or specimen
from port of retention catheter if in place
7. Encourage the client to continue medical supervision and follow up care, including visits
to an eye care specialist and podiatrist
8. Encourage follow-up nutritional counseling
 PLANNING/IMPLEMENTATION
 Teach client and family to:
1. Use blood glucose monitoring system to test blood glucose
2. Test urine for ketones when blood glucose is high
3. Avoid infection
4. Care for the legs, feet, and toenails properly; inspect, bathe, dry; lubricate feet except
between toes, avoid exposure of feet to heat sources, wear shoes to protect feet
5. Administer insulin by using sterile technique, rotating injection sites within an anatomic
location, measuring dosage, noting types, strengths of insulin, and peak action periods, using
insulin pump, need to carry carbohydrate source
6. Use diabetes food guide pyramid and food tables when planning dietary intake
7. Avoid tight shoes and smoking, which will constrict circulation
8. Recognize signs of impending hypoglycemia (insulin, shock, reaction)
9. Recognize signs of impending hyperglycemia (DKA, HHKS)
 EVALUATION/OUTCOMES
1. Complies with medical regimen of diet, exercise, and medications
2. Maintains blood glucose and hemoglobin A1c levels within an acceptable range
MANIFESTASI KLINIK
PROSES NORMAL
DM TYPE 1
DM TYPE 2 (NIDDM)
KOMPLIKASI AKUT DM
KOMPLIKASI KRONIS DM
 ASUHAN KEPERAWATAN PADA KLIEN
DENGAN MASALAH KELENJAR ADRENAL
CUSHING’S SYNDROME

 Data Base
A. Etiology and Pathpphysiology
1. Results from excess secretion of adrenocortical hormones
2. Caused by hyperplasia or by a tumor of the adrenal cortex; however, the primary lesion may
occur in the pituitary gland, causing excess production of ACTH
3. Administration of excess glucocorticoids or ACTH will also cause Cushing’s syndrome
 B. Clinical findings
1. Subjective: weakness; decreased libido; mood swings; steroid psychosis
2. Objective:
a. Obese trunk, thin arms and legs; moon face; buffalo hump; acne; hirsutism, ecchymotic areas, purple
striae on breast and abdomen; amenorrhea, increased susceptibility to infections
b. Hypertension
c. Hyperglycemia; hypokalemia; elevated plasma cortisol level
d. Elevated 17 hydroxycorticosteroids and 17-keyosteroids in urine
e. Osteoporosis, fractures, kyphosis
f. Protein wasting, which causes muscle wasting and weakness
g. Sodium and water retention with edema and hypertension
Therapeutic Interventions
1. Reduce dosage of externally administered corticoids
2. If lesion on pituitary is causing hypersecretion of ACTH, a hypophysectomy or irradiation
of the pituitary may be done
3. Surgical excision of adrenal tumors (adrenalectomy)
4. Adrenal enzyme inhibitors
5. Potassium supplements
6. High-protein diet with sodium restriction
Nursing Care of Clients with Cushing’s Syndrome
 ASSESSMENT
1. Baseline vital signs, weight, blood glucose and electrolytes
2. Urine specimens for diagnostic purposes
3. Physical appearance
4. Changes in coping and sexuality from history
 NURSING DIAGNOSES
1. Disturbed body image related to altered appearance
2. Excess fluid volume related to sodium excess
3. Risk for infection related to altered immune response
Nursing Care of Clients with Cushing’s Syndrome
 PLANNING/IMPLEMENTATION
1. Monitor vital signs, daily weight, intake and output, blood glucose, and electrolytes
2. Protect the client from exposure to infections
3. Encourage ventilation of feelings by the client and spouse because changes in body image and sex drive can alter
spousal support
4. Attempt to minimize stress in the environment by measure such as limiting visitors and explaining procedures
carefully
5. Instruct client regarding diet and supplementation; encourage diet rich in nutrient-dense foods such as fruits,
vegetables, whole grains, and legumes to improve and maintain nutritional status and prevent any possible drug-
induced nutrient deficiencies
6. Care for the client following a bilateral adrenalectomy
7. Care for the client following a hypophysectomy
 EVALUATION/OUTCOMES
1. Maintain fluid balance
2. Remain free of infection
3. Discusses feeling regarding physical change
ADDISON’S DISEASE

DATA BASE