Nursing care of client with endocrine system disorder

Endocrine - Made up of gland in many tissues & organs in diff. body areas– Main feature of all endocrine gland is the secretion of hormones-Maintenance and regulation of vital functions-Response to stress injury-Growth and development-Energy metabolism-Reproduction-Fl & elec., acid base balance

Hormones- Are natural chemical

substances that initiate or regulate activity and exert their effect on specific tissues known as Target tissues.

Target Tissue- Are usually located some distance

from the endocrine gland with no direct physical connection bet. the endocrine gland & its target tissue. Then endocrine gland are called “ductless” gland and must be used the blood to transport secreted hormones to the target tissue.

Negative Feedback- The level of hormone in the blood is

regulated by the homeostasis called Negative feedback

Ex: control of insulin secretion- Inc level of bld glucose, the hormone

insulin is secreted thus inc glucose uptake by the cells ->causing a dec in bld glucose.

The FF: Endocrine Gland1. Islets of

langerhans:Pancreas2. Pituitary Glands3. Adrenal Gland4. Thyroid gland5. Parathyroid gland6. Gonads

Pancreas- Located posterior to the liver; it influence

Carbohydrate metabolism; indirectly influence fat and protein metabolism; produces insulin and glucagon

1. Glucagon- raises blood glucose

2. Insulin – lower blood glucose

3. Somatostatin – inhibits secretion of insulin, glucagon, and growth hormone from the Anterior pituitary and gastrin from the stomach

Anterior Pituitary1. TSH- thyroid stimulating hormone –

stimulates thyroid growth and secretion of the thyroid hormone

2. ACTH- Andrenocorthropic hormone – stimulates adrenal cortex growth and secretion of glucocorticoids

3. GH-growth hormone – stimulate growth

4. Prolactin or lactogen – Stimulate breast development during pregnancy and milk secretion after delivery

AnteriorPituitary Glands

5. FSH-Follicle stimulating hormone – stimulates ovarian follicles to mature and produce estrogens; in the male stimulates sperm production

6. LH-luteinizing hormone – Acts with FSH to stimulate estrogen production; causes ovulation; stimulates progesteron production by corpus luteum; in male stimulate testes to produce testosterone

7. Melanocytes stimulating hormone – synthesis and spread of melanin in the skin

Posterior pituitary1. ADH Antidiuretic hormone – stimulate

water retention by kidneys to decrease urine secretion

2. Oxytocin – stimulate uterine contraction, causes breast to release milk into ducts

Thyroid gland1. Thyroid hormone(thyroxine T4 and

TriidothyronineT3) – increases metabolic rate

2. Calcitonin – decreases blood calcium concentration

Adrenal Medulla1. Epinephrine( adrenalin) – prolongs and

intensifies sympathetic nervous response to stress

2. Norepinephrine – prolongs and intensifies sympathetic nervous response to stress

Diagnostic evaluation with endocrine disorder

Laboratory studies:1. Test of thyroid – to differentiate primary and

secondary hypothyroidism2. Serum thyroid-stimulating hormone – to measure

the basal serum thyroid-stimulating hormone concentration

3. Serum thyroxine and triiodothyronine – to measure concentration of thyroxineT4 (T3) in the blood

4. Test of parathyroid function – to measure the concentration of calcium, phosphorus, alkaline, phosphatase, parathyroid hormone and osteocalcin in the blood

Diagnostic evaluation with endocrine disorder

5. Test of adrenal function – to measure concentration of adrenocortical hormones and adrenal medullary hormones through urine and blood specimen

6. Aldosterone levels – aids in the diagnosis of hyperaldosteronism

7. Urine catecholamines – to assess function of the adrenal medulla

Diagnostic imaging and other studies

• Test for thyroid structure & function – to assess the size, shape, position, and function of the thyroid through ultrasound, MRI, CT scan, & radionuclide imaging

• Radioactive iodine Uptake – to measure the amount of radioactive iodine in the thyroid 24h after administration of a radioiodine isotope through scintillation scanner

• Achilles Tendon Reflexes – to diagnose thyroid disorders by measuring the amplitude and duration of ankle jerk using an instrument that will help to elicit the reflex

Care of patient with Pituitary DisordersHYPERPITUITARISM- Oversecretion of hormone due to tumor

or hyperplasia -> compresses brain tissue -> neurologic S&S: ICP, Visual changes, headache

- Hormone affected: Growth hormone & ADH

- Resulting to Gigantism if the secretion occurs in childhood; in Adult Acromegaly

a. AcromegalyPathology:- GH hypersecretion during adulthoodRisk: Pituitary adenomaCardinal Signs: large hands and feet;

protrusion of lower jaw(Prognathism). Coarse facial feature

Nurse Concern: Psychosocial adjustment to Altered body image; monitor Diabetes Insipidus

b. Dwarfism- due to hyposecretion of growth hormoneNursing Intervention:• Assess patient using DDST• Monitor height and weight• Assess other neurologic functions• Focus on the family client’s feelingMedical Mgt:• Biosynthetic growth hormone -

Somatrem

b. Gigantism

- Results from excessive secretion of growth hormone

Clinical manifestation: Height more than 8 feet Acromegaly

Medical Mgt: Radiation therapy Parlodel Transphenoidal hypophysectomy

Panhypopituitarism (Simmond’s Disease)

-complete absence of pituitary secretion resulting to:

• Dwarfism• Hypoglycemia• Extreme weight loss• Hair loss• Emaciation• Impotence• hypometabolism • absence of gonadal & adrenal function• Atrophy of all endocrine gland and organs

Medical/surgical Mgt

1. Transphenoidal hypophysectomy

2. Stereotactic radiation therapy

3. Bromocriptine

4. octreotide

Nursing Mgt. who Undergone Transphenoidal Hypophysectomy –removal of the Pituitary gland

• Assess inc. ICP & CSF leaks• Monitor seizure and stress ulcer• Elevate head 20 degrees• Apply cool, moist packs over the eyes foe

ecchymosis and periorbital edema• Adm. artificial tears or ointment as ordered• Use sterile technique for all dressing to prevent

meningitis• Do not suction through the nose

Type of hypophysectomy & Ng Consideration

1. Supratentorial surgery – elevate head of the bed to 30 degrees

2. Infratentorial surgery – keep client flat on bed to prevent pressure on the brainstem. Turn q 2 h but never on the back

3. Posterior Fossa surgery – position on either side but never on the back. A pillow may be placed under the head for support, Monitor VS changes since the site close to vital brain stem function, monitor cardiac arrhythmias and air embolism

4. Bony Flap – place the client only on the unoperated side or back

3. Hyperpituitarism- Results from excessive secretion of

hormones produced by the pituitary gland caused by tumor

S&S: Gigantism, acromegalygalactorrhea,Visual field abnormalities, headache

Surgical Mgt:

- Removal of the tumor

Hyperprolactinemia

- Results from oversecretion of prolactin associated with pituitary tumors

- Mgt and Ng Mgt same as hyperpituitarism

Nursing Intervention after surgery

• Monitor VS

• Monitor LOC

• Orient to time, place and person

• Check response to stimuli

• Assess visual acuity

• Monitor hormonal insufficiencies

• Monitor ICP

4. Hypopituitarism- Result from destruction of the anterior pituitary

gland, hypothalamic dysfunction, trauma, tumor, vascular lesion, and complication of radiation therapy to the head and neck area

S&S:- Extreme weight loss Emaciation- Hypoglycemia Impotence- Amenorrhea Hypometabolism

5. Pituitary tumorTypes:1. Eosinophilic – result to gigantism if developed early in

life and acromegaly if developed during adult life2. Basophilic – results to cushing’s syndrome; clinical

manifestation: amenorrhea & masculinization in females, truncal obesity, HTN, osteoporosis & polycytemia

3. Chromophobic – produces no hormone but destroys the whole pituitary glands resulting to hypopituitarism. S&S: obesity, somnolence, scanty hair, dry, soft skin, loss of libido, headache, blindness, polyphagia, polyuria, and lowered BMR

6. Gonadal Disorder

- Result from hypothalamic-pituitary dysfunction resulting to hyposecretion of gonadotropins may lead to infertility and hypoandrogenism

- Collaborative Mgt:

- Removal of the underlying cause of pituitary dysfunction

Posterior Pituitary Disorders

1. SIADH Syndrome of Inappropriate Antideuritic Hormone – resulting from abnormal increase of ADH secretion & excessive water retention leads to inc urinary sodium

Etiology:Bronchogenic carcinoma, head injury, tumor, infection, and

brain surgeryCardinal signs: water intoxication, neurologic signsMedical Mgt:• Diuretics & Demecclocycline (declomycin)• Eliminate underlying cause

Nurse Concern

• Check daily weight

• Oral fluid restriction, IV with hypertonic solutions

• Monitor I&O & weight

• Assess client’s neurologic status

• Monitor urine and blood chemistries

2. Diabetes Insipidus- A condition characterized by a defficiency

in antideuritic hormone resulting to excessive fld excretion: neurogenic and nephrogenic

Risk: head trauma, irradiation, removal of pituitary gland, renal disease

Manifestation: diluted urine, polydipsia, excessive urination

Dx: vasopressin and H20 deprivation test; serum Na inc &UA

Cardinal signs: Polyuria, Polydipsia

2. Diabetes InsipidusMedical Mgt:- Vasopressin/petressin replacement

(desmopressin)- Thiazide diuretics- Chlorpropamide (diabinese)- Clofibrate (Hypolipidemic agent)- Advice the client to wear a medical alert

bracelet- IV hypotonic; MIO, weight, low Na & no

caffeine

Care of patient with Abnormal thyroid Function

1. Hypothyroidism/myxedema – due to decreased thyroid hormone concentration in the blood result in hypometabolism: cretinism, myxedema, iodine dficiency, Hashimoto’s thyroiditis

Risk: congenital, elderly, infection, iodine deficiency, antithyroid medication, undiagnosed

Dx: Inc TSH, dec T3T4; dec RAIU with thyroid suppression test

Cardinal Signs• Cold intolerance Non-pitting edema• Anorexia All symptoms are dec• Fatigue mask-like face

Medication: Levothyroxine; Synthroid, Liotrix, IV glucose for hypoglycemia

Nurse Concern:• Monitor both hypo &hyper symptoms• Monitor VS, weight and toxicity• Avoid cabbage, carrots, spinach, turnips and

peaches

Hyperthyroidism/GRAVES’ DISEASE

Pathology: due to excessive secretion of TH -> oxygen consumption & heat production: Grave’s, Parry’s’ Baseow’s, Exophthalmic goiter, toxic diffuse goiter

Risk: stress, injury, infection, surgery, female, immunologic, excessive pro-thyroid meds

DX: dec TSH inc T4T3, Inc RAIU with thyroid suppression test

Cardinal signs:• Heat intolerance inc appetite• All symptom elevated except weight, sex drive, fluid

volumeS&S: “ thyroidism”T- tremor I-intolerance to heatH-heart rate up D- diarrheaY-yawing/fatigability I irritabilityR- restlessness S- sweatingO-oligomenorrhea &amenorrhea muscle wasting

&wt. loss

DOC: “i met a pro”: Methimazole(tapazole) & Propylthiouracil (PTU)

Nursing Intervention:

Nursing interventions• Monitor VS• Advice to wear eye patch during night if

exompthalmus is present• Advice to wear sunscreen

• Keep environmental cool

• Caloric requirement is 4000 – 5000/day

• Post op care: thyroidectomy; monitor complications: hemorrhage, respi distress, laryngeal nerve damage & tetany

Thyroiditis- Inflammation of the thyroid glandS &S: Pain & swelling of the anterior neck Pharyngitis or pharyngeal pain Dysphagia DysphoniaDOC: ORAL CORTICOSTEROIDS; NSAID’s; antimicrobialCollaborative Mgt: Surgical incision & drainage Fluid replacement Avoid ASA coz it displaces thyroid hormone from its

binding sites and inc the amount of circulating hormone

Thyroid tumors- Classified as benign or malignant, on

the basis of the presence or absence of associated thyrotoxicosis

Types:

1. Endemic goiter – iodine-deficit goiter mostcommon type as caused by iodine deficiency

2. Nodular – nodules inc in size, with some descending into the thorax

Medical/surgical Mgt• Thyroidectomy• Anticoagulants are stopped several weeks

before surgery

Nursing Intervention:

Preop:• Prepare quite and relaxing forms of

recreation/occupational therapy• Teach the importance of a diet in CHO &CHON• Demonstrate how to support the neck with the

hands to prevent stress on the incision

Postop care

• Position the patient in the most comfortable position (semi-Fowlers)

• Manage pain• Assess the surgical dressing periodically &

reinforce when necessary• Monitor VS• For indication of bleeding, and sensation of

fullness at the incision site• Assist patient to eat foods that are easily eaten• Prescribe a well-balanced diet, high calorie to

promote wt gain

Care of client with abnormal parathyroid Function

1.Hypoparathyroidism – hyposecretion of parathyroid hormone by the parathyroid gland

S&S:• latent tetany: numbness, tingling, cramps,

stiffness of hands and feet• Overt tetany: bronchospasm, lyngospasm,

photophobia, dysrhythmias, hyperphosphatemia

• Anxiety, irritability, depression, delirium• Positive Chvostek’s signs & trousseau’s signs• Thin, patchy hair, brittle nails, dry scaly skin• Cataract formation

Medical & Surgical Mgt:

• Elevate the serum calcium level to 9 – 10mg/dl• Calcium gluconate IV in Hypoparathyroidism &

Hypocalcemia• Parenteral parathormone, bronchodilators,

Phenobarbital• Tracheostomy or mechanical ventilation• High calcium, low phosphorous diet• Oral calcium salts, aluminum hydroxide gel or

aluminum carbonate• Vit D

Nursing Intervention:

• Closely monitor for allergy to parathormone• Instruct to avoid milk, amd milk products,

eggyolk, spinach• For acute Hypoparathyroidism:

Administer IV calcium gluconateMonitor hypocalcemiaa, tetany, seizure, & respi

distressMonitor for convulsion & protect from injuryMonitor for cardiac ArrhythmiasAdminister calcium supplement & Vit D as prescribed

2. Hyperparathyroidism

Pathology: inc PTH -> Hypercalcemia & hypophosphatemia -> bone decalcification, renal calculi, metabolic acidosis (from inc CHO3 excretion)

Risk: elderly, female, thyroid adenomaDX: Serumcalcium, & Phosphorous incCardinal Signs: bone painS&S:• Backache, joint pain, Polyuria, Polydypsia• Kidney stone,Nausea, anorexia, constipation• Abdominal pain, restlessness, depression,

irritability, neurosis, psychosis

Medical & surgical Mgt:

• Hydration therapy

• Loop diuretics, furosemide – promote renal calcium secretion

• Avoid thiazide diuretic – can inc calcium level

DOC: “calci, you’re such as Pig”( calcitonin, plicamycin, IV saline, Gallium nitrate – inhibit bone resorption

Nursing intervention• Encouraged fluid intake up to 3000ml/day

• Encouraged low calcium, low Vit D

• Monitor VS, cardiac dysrhythmias

• Assess skeletal pain

• Monitor I&O/ ECG

• Monitor calcium & phosphorous level

• Strain urine

Care of Client with Abnormal Adrenal functions:1. Addison’s disease

Pathology:– chronic adrenocortical insufficiency -> hypovolemia -> shock(Addison’s crisis)

Risk: immunologic, removal of adrenals,infection and tumor of adrenals,m head rauma affecting pituitary withdrawal of corticoids

DX: dec serum cortisol, dec sodium, Inc potassium and dec aldoterone; ECG (peaked T wave), ABG (acidosis)

Signs and Symptoms:

Cardinal signs: Hyperkalemia, “bronze skin”. Fatigue, diarrhea

• Muscle weakness, fatigue

• bronzed skin: knuckles, knees, elbows, mucous membrane

• Anorexia, wt loss, emaciation

• Postural hypotension, stress

DOC: cortisone or florinef; IV glucocorticoid; fluid with Na

Nursing Interventions• Instruct patient to report inc thirst• Provide Na and high in CHO & CHON• Educate lifelong adrenal cortex hormone replacement• Avoid beverages or foods with caffeine• Instruct patient to avoid strenuous exercise in hot &

humid environment• Avoid OTC medication• Avoid individual with infection• Monitor VS• Monitor blood glucose, & Potassium levels• Maintain bed rest and provide a non stimulating

environment• Monitor I&O• Monitor neurologic status

2. Adrenocortical Hyperfunction

a. Cushing syndrome

Pathology: Hypercortisolism/ hypersecretion of glucocorticoids and androgens due to overactivity of the adrenal gland

Etiology: Pituitary tumors excessive corticosteroids

DX: serum cortisol, Na, K+ and glucose; ACTH/ dexamethasone suppression test

Signs & SymptomsCardinal signs: psychosis, “Buffalo hump”, truncal

obesity with slender limbs, hirsutism, hypernatremia. “moon face”

S&S:• Muscle wasting, osteoporosis, kyphosis,

backache, fractures• Hypokalemia, metabolic alkalosis• Hypertension. CHF• Skin oiliness, acne• Inc susceptibility to infection, dec resistance to

stress• Poor wound healing• Menstrual irrigularities, loss of libido

Medical/Surgical Mgt:• Radiation therapy for pituitary tumors

• Cytoxic antihormonal agents

• Hydrocortisone therapy

• lifetime replacement of adrenal cortex hormones

• Adrenal enzyme inhibitors

• Transphenoidal hypophysectomy

• adrenalectomy

Nursing intervention• Provide High protein, calcium and Vit D

and low NA, CHO and calories • Promote rest and activityNsg. Intervention after transphenoidal

hypophysectomy• Assess for signs of cerebral edema and

rising of ICP• Assess for signs of meningitis• Observe client for rhinorrhea after nasal

packing removed

b. Hyperaldosteronism or Conn’s syndrome)

Pathology: excessive secretion of aldosterone by the adrenal cortex of the adrenal gland,caused by adenoma

S&S:

• Headache, fatigue, muscle weakness

• Polydepsia, polyuria, paresthesis, visual changes, hypernatremia’ low urine specific gravity

• Increased urinary aldosterone

Nursing Intervention

• Monitor VS particularly BP

• Monitor hypokalemia

• Monitor I&O & urine specific gravity

• Administer potassium-sparing diuretics

• Administer antihypertensive as ordered

• Prepare client for adrenalectomy

3. Adenomedullary disorders

1. Pheochromocytoma

Pathology: catecholamine-secreting tumor of the adrenal medulla; excessive secretion of epinephrine and norepinephrine

Risk: genetics, middle age

S&S:

Cardinal signs: 5H’s:HTN, Headache, Hyperglycemia, Hyperhidrosis(excessive sweating, Hypermetabolism

S&SAcute attack: profuse diaphoresis,dilated

pupil, and cold extremities, extreme anxiety and weak, headache, vertigo, blurring of vission, tinnitus, air hunger, dyspnea, feeling of impending doom, palpitations, tachycardia

-Clonidine suppression test reveals no change in cathecholamine levels

Medical /Surgical MGT• Alpha-adrenergic blockers –phentolamine• Smoothes muscle relaxants-Na

Nitroprusside for HNT• Beta-adrenergic blockerNursing Intervention:• Standard pre/post op care• Monitor BP,UO,glucose & ketones &

neurologic signs• Seizure precaution. Provide high CHO, Vit

and minerals

Pancreas

• Lies horizontally behind the stomach at the level of the 1st and 2nd lumbar vertebrae

• The head attached to the duodenum, tail reaching to the spleen

• With exocrine and endocrine function

• Produced two Impt. hormones:1. Insulin: beta cells of islets of Lagerhans –

Decrease glucose levels: transcellular membrane transport of glucose; inhibits breakdown of fats and protein; requires Na for transport pf CHO; requires K for production

Glucagon

• Alpha cells of Islets of Lagerhans

• Stimulates release of glucose by the liver

• Increases glucose levels (gluconeogenesis)

Diabetes mellitus• A chronic systemic disease characterized by

disorder of CHO, CHON and fats

Classifications:

1. Type 1: IDDM; Juvenile onset; Brittle; labile;

2. Type 2: NIDDM; Adult onset

3. Other Specific Types: beta cell genetic defect; endocrinopathies, drug/chemical induced

4. Gestational Diabetes mellitus

Diagnostic test

1. FBS: 80 – 120mg/dl- DM: Incr. 140 for 2 readings2. 2 h PPBS: initial bld is withdrawn , 100g of CHO diet,

2h after meal bld specimen is withdrawn – bld sugar returns to normal level

3. OGTT/GTT: initial urine & bld specimen are collected, 150-300g of CHO/po, series of bld. specimen is collected: 30min, 1h, 2h-S.CHO return to normal, 3, 4, 5 h as required; done when result of FBS/ 2h PPBS are borderline

4. Glycosylated Hgb: most accurate; reflects s. CHO level for the past 3 -4 mos: excess glucose in the bld->attaches to Hgb-> hgb lifespan 90 – 120 days

Predisposing Factors• Stress – stimulates secretion of epinephrine,

noeepiniphrine, glococorticoids increases CHO

• Heredity – type 11 DM• Obesity – adipose tissues are resistant to

insulin ->glucose uptake by the cell is poor• Viral Infection – increase risk to autoimmune

disorders• Autoimmune disorder – type 1 DM• Women - multigravida

Pathophysiology

- Insulin Deficiency -> Hyperglycemia: a. -> Inc.bld osmolarity = ICF dhn b. Glycosuria -> glucose level exceeds renal threshold (180mg/dl) c. Polyuria - > glucose exerts high osmotic pressure within the renal tubules ->osmotic diuresis occurs - > hypovolemia ->ECF dhn. d. Polydipsia -> result from ECF/ICF dhn. e. Inc bld viscosity - > sluggish circulation -. Proliferation of microorganism - > infections. f. Polyphagia – the cell are starved. - > inc lipolysis: -> a. Hyperlipidemia -> Atherosclerosis: Macroangiopathy: in brain – CVA, Heart – MI, Peripheral arteries PVD’s( Peripheral vascular Disease); Microangiopathy: Kidneys – RF, Eyes Retinopathy/cataract; Neuropathy: spinal cord/Autonomic Nervous system, paralysis, Gastroparesis, neurogenic bladder, dec libido, impotence, peripheral neuropathy, numbness /tingling b. Ketonemia: Acetone, aceto-acitic acid, beta-hydroxy-butyric acid -> dec bld pH-KETOACIDOSIS -> Ketonuria -> inc, CHON breakdown -> a. (-) Nitrogen balance b. Inc BUN, s creatinine c. Tissue wasting d. Weight loss e. Debilitation

Comparison of clinical manifestation of type 1 and type 2

Type 1 Type 2Etiology-----------Autoimmune--------------genetic, obesityAge of onset -----rare before age 1--------incr with age% of diabetics-----5 -10% -----------85 – 90%Onset ---------------Abrupt, rapid ------------gradual, over yrsBW at Onset ------normal or thin ----------80% overweightInsulin Production ---None ------------------less, normal, greaterInsulin Injection ------always ----------------30% are requiredKetosis -------occurs mainly in children ---unlikely

& adolescenceMgt. ----------insulin, diet, exercise -------diet, weight loss,

exercise, oral or insulin

Signs & Symptoms

• Cardinal Signs: Polyuria, Polydipsia, polyphagia, Hyperglycemia (for type1: weight loss; type 2: weight gain)

• Vision changes

• Tingling, numbness in the hands/ feet, slow healing sores

• Fasting Plasma Glucose > 126mg/dl

• Random plasma glucose levels>200mg/dl

Medica/Surgical Mgt

Five components in Diabetes Mgt:

1. Nutrition/diet therapy

2. Exercise

3. Monitoring

4. Pharmacologic therapy

5. Education

• Insulin therapy

• Pancreas transplant

Nursing intervention

• Encourage weight loss• Instruct patient not to skip meals• Monitor CHO intake• Reduce saturated fats & cholesterol intake• Increase dietary fiber intake• Provide exchange list for meal planning• Limit alcohol intake• Educate about urine ketones testing, normal

blood glucose range and medication• Educate on the method of self-monitoring of

blood glucose

Acute Complication of Diabetes

a. Hyperglycemia & Diabetic ketoacidosis – absent/ markedly inadequate insulin production

Three main Clinical features:

1. Hyperglycemia

2. Dehydration and electrolytes loss

3. Acidosis

Causes of DKA & Hyperglycemia

• Taking too little insulin

• Omitting doses of insulin

• Developing insulin resistance due to insulin antibodies

• Failing to meet increased need for insulin due to infection, surgery, trauma, pregnancy or puberty

DKA VERSUS HHNSCharac: DKA HHNSPatient affected type1 or 2 type1 0r 2

more in type1 more in typePrecipitating omission of insulin, physiologic stress event stress physiologic infection, surgery

CVA, MI,surgery MI, CVAOnset rapid< 24hr slower- daysBld glucose level >250mg/dL >600mg/dL

>13.9mmol/L >33.3mmol/LArterial pH <7.3 normalSerum&urine ketones present absentSerum osmolality 300-350mOsm/L >350mOsm/LPlasma bicarbonate <15 mEq/L normalBUN & creatinine Elevated elevatedMortality rate <5% 10 to 40%

Sign& Symptoms• Warm dry skin, nausea & vomiting

• Flushed appearance, dry mucous membrane, soft eyeballs

• Kussmaul’s respiration, fruity or acetone odor of the breath

• Alteration in LOC, Hypotension

• Polyuria early sign

• Oliguria late sign

Medical Mgt:

• Fluids & electrolytes replacement – K+• Continuous insulin infusion

Nursing Intervention:• Monitor blood glucose q 1 – 2 h• Monitor LOC & neuro status and notify• Monitor sign of hypo & hyperkalemia• Monitor I&O• Watch out for signs of fld overload• Monitor for signs of ICP

b. HHNS – Hyperglycemic Hyperosmolar Non-Ketotic Syndrome

Pathology: a variant of diabetic ketoacidosis characterized by extreme hyperglycemia, mild or undetectable ketonuria and absence of acidosis. Often see in aging clients with NIDDM

Precipitating factor:

• Stress, infection, medication: thiazide, diuretics, steroids, phynetoin

Signs & symptoms

• 3Ps, glucosuria,dehydration, hyperpyrexia

• Abdominal discomfort, hypotension, shock, hyperventilation, neurologic signs

• Seizures, tachycardia

MEDICAL Mgt:

• Fluid & Electrolytes replacement

• Insulin therapy

C. HYPOGLYCEMIA

Pathology: blood glucose levels <60mg/100ml

SIGNS & SYMPTOMS:

• Tachycardia, headache, weakness, irritability

• Lack of muscular coordination

• Night hypoglycemia, Bizarre nightmares, restlessness, diaphoresis

• Sleeplessness, confusion

Nursing Intervention

Mild hypoglycemia• Administer fast acting sugar• Perform blood glucose test at the onset of

symptoms• Retest the blood glucose in 15 – 30 min.& treat

again if the blood glucose is not over 100mg/100ml

• Instruct to carry simple sugar at all time• Instruct to refrain from eating high-calorie, high

fat dessert foods in treating hypoglycemia

Hypoglycemia in Unconscious or Semiconscious

• Glucagon may be given im or subcu• 20 – 50 ml of 50% glucose bolus• A longer acting CHO and CHON snack

should follow either of the above tx once pt. is awake

1.Hypoglycemic Unawareness- A syndrome wherein the diabetic patient is

unaware that he/she is hypoglycemic- Absence of clinical manifestation when

glucose level is less than 55mg/dl

2. Hypoglycemia with rebound hyperglycemia

• Known as SOMOGYI Phenomenon – result from excessive evening dose of insulin

• Hypoglycemia occurs at around 2 – 4 AM which causes an increase in the production of counterregulatory hormones and increase production of glucose in the liver

• tx include the bedtime snack and dec the evening dose of intermediate-acting insulin

3. Dawn Phenomenon

• Refers to an early-morning(4-8am) increase in the blood glucose level

• May cause by wearing off of insulin and nocturnal release of growth hormone

Chronic complication of DMA. coronary artery disease

- Due to diposition of lipids to the inner layer of the vessel walls

- Most common cause of death in DM pt

B. Cerebrovascular disease

- Most common and severe in DM pt

- Manifested by TIA and stroke

- Most common form: atherothromboembolic infarction

C. HTN - HYPERTENSION

- A major risk factor for the development of stoke and nephropathy

D.PERIPHERAL VASCULAR DISEASE- Total or partial occlusion of the blood vessels

resulting to deprivation of O2 and other nutrients to the extremities

- May lead to the development of intermittent claudication, absent pedal pulses, ischemic gangrene, sensory and autonomic neuropathy and inc risk of infection

e. INFECTION

-Slow progression of wound healing due to damage blood vessel

- 3 factors to the development of infection in DM Pt;

1. Polymorphonuclear leukocyte function

2. Neuropathies

3. Vascular insufficiency

Microvascular complicationa. Diabetic retinopathy – chronic and

progressive impairments of the retinal circulation characterized by blurring of vission sec. to macular edema

S&S: microaneurysm, intraretinal hemorrhage, hard exudates including sp, macular edema, blurry vision, floaters, cobwebs in the visual field, sudden visual changes , hazy vision, complete vision

Mgt: Argon laser photocoagulation. Vitrectomy, maintain safety, control HTN and glucose level

B. Nephropathy

- Renal disease due to diabetic microvascular changes in the kidney

S&S: albuminuria, anemia, thirst, frequent UTI, fatigue, malnutrition, weight loss

Mgt:

- Maintain bld glucose level

- Control HTN, low Na & low CHON

- Treat infection; I&O

- Monitor BUN and Creatinine albumin level

NEUROPATHY

- Deterioration of the nervous system throughout the body

S&S: paresthesias, dec or absent reflexes, dec. sensation, burning sensation in the LE, poor peripheral pulses, dizziness, and postural hypotension, incontinence

NG. Intervention:

- Monitor VS, bld. glucose level, foot care, bladder training, administer analgesic as prescribed

Categories of Insulin• Lispro (Humalog) – rapid acting - onset-10 -15

min - duration – 3h – indication used for rapid reduction of glucose level, to treat postprandial hyperglycemia & to prevent nocturnal hypoglycemia

• Aspart (Novolog) -rapid acting – onset 10 to15 min – peak 40 to 50 min. duration – 4 to 6 hr indication same as Lispro

• Regular (Humalog R, Novolin R, Iletin 11 regular I short acting – onset ½-I hr – peak 2-3 hr – duration 4 to 6hr – usually administered 20 30 min. AC; may be taken alone or in combination with longer acting Insulin

Categories of insulin

• NPH(NEUTRAL PROTAMINE Hagedorn –onset – immediate acting – onset – 2-4hr peak 6- 12h duration – 16 20hr – usially taken PC

• Humulin N, Iletin11 lente,iletin11 NPH NOvolin L (Lente), Novolin N (NPH) immediate acting – onset -3- 4 hr, peak – 6 -12hr, duration – 16 – 20 hr usually take with food

Insulin categories• Ultralente(UL) –long acting,onset-6 to8 hr

,peak- 12 -16 hr, duration 20-30hr, used primarily to control fasting glucose level

• Glargine (Lantus) very long acting, onset iht, peak contionus no peak, duration 24 hr, used for basal dose

Complication of insulin therapy• Local allergic reaction – redness, swelling

tenderness• Systemic allergic reaction- local skin

reaction• Insulin lipodystrophy – localized reaction

in the form of either lipoatrophy( loss of subcutaneous fats and appears as slight dimpling or more serious pitting of subcutaneous fat) or lipohypertrophy( development of fibrofatty masses at the injection site

Insulin complication• Insulin resistance – common for obesse

patient, and immune antibodies develop and bind the insulin

• Morning hyperglycemia – insufficient level of insulin due to: dawn phenomenon – (bld glucose begin to rise), Somogyi effect( nocturnal hypoglycemia followed by rebound hyperglycemia), insulin frequently seen in the evening waning