CARE OF CLIENTS WITH DISORDERS IN THE ENDOCRINE SYSTEM

I. Hormones
T HYROID – STIMULATING HORMONE (TSH)
Aka THYROTROPIN
STEROIDEx.HORMONES
Hydrocortisone
Produced by THYROTROPES or thyrotropic cells of the APG
Hyposecretion: SECONDARY HYPOTHYRODISM
P Ex. Insulin
EPTIDE / PROTEIN HORMONES Hypersecretion: SECONDARY HYPERTHYROIDISM

AMINEEx.HORMONES
Epinephrine P ROLACTIN (PRL)
Aka MAMMOTROPIN
Produced by MAMMOTROPES or mammotropic cells of the
II. Endocrine Glands APG
A. Major Endocrine Glands Hyposecretion: POOR MILK SECRETION
1. Pituitary gland
Hypersecretion: GALACTORRHEA, IMPOTENCE (males),
2. Thyroid gland AMENORRHEA (females)
3. Parathyroid glands
4. Pancreas
5. Adrenal glands
6. Ovaries – Estrogen & Progesterone
ADRENOCORTICOTROPIC
Aka CORTICOTROPIN
HORMONE (ACTH)

Produced by CORTICOTROPES or corticotropic cells of the

7. Testes - Testosterone
APG
8. Hypothalamus – GHRH, GHIH, TRH, PIH, CRH, GnRH, Hyposecretion: SECONDARY ADDISON’S DISEASE
MIH, Oxytocin, ADH Hypersecretion: SECONDARY CUSHING’S DISEASE
B. Minor Endocrine Glands
1. Thymus - Thymosin
2. Pineal gland - Melatonin
C. Other tissues
L UTEINIZING HORMONE (LH)
&
1. Placenta – HPL, HCG
2. GIT – Gastrin, Secretin, Cholecystokinin F OLLICLE-STIMULATING HORMONE (FSH)
3. Kidneys – Erythropoietin
Aka GONADOTROPINS
III. Diagnostic Test Groups Produced by GONADOTROPES or gonadotropic cells of the
A. Blood Tests APG
1. determines hormone blood levels Hyposecretion: HYPOGONADISM, SEXUAL
2. Detects antibodies MATURATION INHIBITION
3. Assesses effect of hormone on other substances (e.g., Hypersecretion: HYPERGONADISM, PRECOCIOUS
insulin on glucose) PUBERTY
Ex. Radioimmunoassays
B. Urine Tests – measure amount of hormone or end products of
hormones excreted by the kidneys
Ex. Vannillylmandelic acid test for pheochromocytoma
MELANOCYTE-STIMULATING HORMONE (MSH)
Believed to be secreted by the Intermediate lobe of the APG
C. Stimulation or Suppression tests Has a stimulating effect on the Adrenal Cortex Affects
1. Stimulation tests – administration of stimulating pigmentation
hormones Hyposecretion: ALBINISM
(+) response = problem in hypothalamus or pituitary gland Hypersecretion: ETERNAL TAN
(-) response = problem in endocrine gland itself
2. Suppression tests – used to determine whether negative B. POSTERIOR PITUITARY GLAND (PPG) – aka
feedback mechanisms that normally control secretion of NEUROHYPOPHYSIS
hormones from hypothalamus or pituitary gland are intact - Does not produce its own hormones
- Hormones of PPG are produced by the Hypothalamus
IV. PITUITARY GLAND – aka HYPOPHYSIS; located at the sella - PPG stores and releases these 2 hormones
turcica at the base of the brain, overlying the sphenoid bone; located
behind the optic chiasma and optic nerves. OXYTOCIN
- Necessary for uterine contraction and milk
A. ANTERIOR PITUITARY GLAND (APG) – aka ejection (milk let-down reflex)
ADENOHYPOPHYSIS
- Produces its own hormones
- Hormones of APG are regulated by RELEASING AND
ANTIDIURETIC HORMONE (ADH)
Aka VASOPRESSIN
INHIBITING HORMONES/FACTORS from the Causes water reabsorption in the kidneys Hyposecretion:
HYPOTHALAMUS DIABETES INSIPIDUS (DI) Hypersecretion:
- Made up of 5 CELLS, each cell producing a distinct SYNDROME OF INAPPROPRIATE
hormone ANTIDIURETIC HORMONE (SIADH)
- Collectively, hormones of the APG go with the
mnemonic GTPALFM for easy memorization C. ENDOCRINE PROBLEMS OF THE PITUITARY GLAND

G ROWTH HORMONE (GH)

Aka SOMATOTROPIN
1. HYPERSECRETION / OVERSECRETION:
HYPERPITUITARISM
Produced by SOMATOTROPES or somatotropic cells of a. Commonly involves ACTH and/or GH
the APG b. CUSHING’S SYNDROME and/or ACROMEGALY
Hyposecretion: DWARFISM / GIANTISM
Hypersecretion: GIGANTISM or ACROMEGALY
 2. HYPOSECRETION / UNDERSECRETION: o Postop interventions:
HYPOPITUITARISM - Monitor V/S, neuro status, LOC, inc.
a. Commonly involves all APG hormones ICP, bleeding, CSF leak (postnasal
b. A rare condition would include all pituitary drip or nasal drainage), electrolytes
hormones, a condition known as for temporary DI or SIADH resulting
PANHYPOPITUITARISM or from ADH disturbances, I & O
SIMMOND’S DISEASE - Elevate the head of bed
- Instruct the client to avoid sneezing,
D. COMMON ENDOCRINE DISORDERS OF THE PITUITARY coughing, and blowing the nose
GLAND - Avoid water intoxication
- Administer glucocorticoids and
1. ACROMEGALY other hormone replacements as
a. Hypersecretion of GH after epiphyseal plate prescribed
closure at puberty - Administer antibiotics, analgesics,
b. Commonly caused by a GH producing pituitary and antipyretics as prescribed
adenoma (tumor) - Instruct the client in the administration
c. Other causes include non-pituitary tumors in the of prescribed medications, which may
pancreas, adrenal glands, and lungs by either producing include vasopressin (synthetic ADH),
GH or more frequently producing GHRH levothyroxine (Synthroid),
d. Assessment: gonadotropic hormones, growth
 Enlargement of the hands, feet, nose, lips and hormone, and glucocorticoids if the
ears, and a general thickening of the skin entire gland has been removed
 Soft tissue swelling of internal organs, notably the  Drug therapy
heart with attendant weakening of its muscularity, o Somatostatin analogues – given by IM or
and the kidneys, also the vocal cords resulting in a subcutaneous injections; stops GH
characteristic thick, deep voice and slowing of production
speech - lanreotide (Somatuline)
 Generalized expansion of the skull at the - octreotide (Sandostatin)
fontanelle  inhibits gastrointestinal and
 Pronounced brow protrusion, often with pancreatic function  loose
ocular distension stools, nausea, gas, gallstone
 Pronounced lower jaw protrusion with attendant formation which is usually
macroglossia (enlargement of the tongue) and asymptomatic, DM rarely
teeth gapping  can be used as an antidiarrheal
 Hypertrichosis, hyperpigmentation, and due to its inhibiting effect of GI
hyperhidrosis may occur function by increasing
e. Complications: absorption of fluid and
 Severe headache electrolytes in the GIT
 Arthritis and carpal tunnel syndrome o bromocriptine (Parlodel) – in tablet
 Enlarged heart (cardiomegaly) - Side-effects: gastrointestinal upset,
 Hypertension nausea, vomiting, light-headedness
 Diabetes mellitus when standing, and nasal congestion
 Heart failure - Start with a very low dose at
 Kidney failure bedtime
 Compression of the optic chiasm leading to loss - Taken with food
of vision in the outer visual fields (typically - Gradually increase dose to the
bitemporal hemianopia) therapeutic dose
 Increased palmar sweating and sebum o Growth hormone receptor antagonist
production over the face (seborrhea) are clinical - pegvisomant (Somavert) – injected
indicators of active growth hormone (GH) subcutaneously daily or can be injected
producing pituitary tumors. weekly in combination with
f. Management: somatostatin analogues
 The goals of treatment are:  Radiation therapy
o to reduce GH production to normal
2. DIABETES INSIPIDUS (DI)
levels
a. Hyposecretion of ADH caused by strokes or
o to relieve the pressure that the growing
trauma, or may be idiopathic
pituitary tumor exerts on the surrounding
brain areas b. Assessment:
o to preserve normal pituitary function  Polyuria of 4 to 24 L/day
o to reverse or ameliorate the symptoms of  Urine contains NO albumin and/or glucose
acromegaly  Inability to concentrate urine
 Surgical removal of the tumor through  Urine osmolality decreases
HYPOPHYSECTOMY  Urine specific gravity decreases (1.001 to
o Aka pituitary adenectomy 1.005)
o Done either via craniotomy or  Polydipsia, patient craves 2-20 liters/day of
transsphenoidal approach (latter cold water
approach is preferred because it is  Dehydration – dec. skin turgor, dry mucous
associated with fewer complications) membranes
o Complications for craniotomy  Weight loss
- Inc. ICP, bleeding, meningitis,  Hypernatremia
hypopituitarism
o Complications for transsphenoidal
surgery
- CSF leak, infection, hypopituitarism
  Serum osmolality increases
 Fatigue, muscle pain and weakness
 Headache
 Postural hypotension that may progress to
vascular collapse without rehydration
 Tachycardia
c. Diagnosis:
 Fluid Deprivation Test
o Withhold fluids for 8-12 H or until 3% -
5% of body weight is lost
o Patient is weighed frequently during the
test
o Plasma and urine osmolality are measured
at the beginning and at the end of the
test
o STOP IFTACHYCARDIA, EXCESSIVE
WEIGHT LOSS, or HYPOTENSION
develops
 Plasma level of ADH
 Plasma and urine osmolality
o Normal plasma osmolality = 270-300
mOsm/kg water
o Normal urine osmolality = 250-900
mOsm/kg water
d. Management:
 Monitor V/S, neuro, CV status
 Provide a safe environment, particularly for the
client with postural hypotension
 Replace ADH
o DESMOPRESSIN (DDAVP)
- Used for chronic or severe DI
- Synthetic vasopressin without the
vascular effects of ADH
- Intranasal (SPRAYED) through
flexible calibrated plastic tube
- Administered OD/BID or every 12
to 24 H
o VASOPRESSIN TANNATE IN OIL
(Pitressin)
- Used for chronic or severe DI
- IM ADH
- Every 24 to 96 H in the EVENING
for maximum results during sleep
- Vial WARMED or SHAKEN
VIGOROUSLY before
administration
- Rotate sites to prevent
lipodystrophy
- Side-effect: Abdominal cramps
- Caution in patients with CAD;
causes vasoconstriction
o CLOFIBRATE, CHLORPROPAMIDE –
potentiate action of vasopressin; used for
mild DI
 Ensure adequate fluid replacement
 Measure intake and output, weight, serum
osmolality, urine specific gravity
 Identify and correct underlying intracranial
pathology
 Instruct the client to wear a Medic-Alert
bracelet.
3. SYNDROME OF INAPPROPRIATE
ANTIDIURETIC HORMONE (SIADH)
a. Hypersecretion of ADH caused by trauma, stroke,
malignancies (often in the lungs or pancreas),
medications, and stress
b. Assessment:
 Water retention (fluid volume overload)
 Urine osmolality increases
 Urine specific gravity increases
 Weight gain
 Dilutional Hyponatremia / water intoxication
 Serum osmolality decreases
 Hypertension
 Altered level of consciousness, cerebral
edema
 Tachycardia
 Anorexia, nausea, vomiting
c. Diagnosis:
 Blood tests: inc. ADH, dec. serum osmolality, dec.
Na (<135 mEq/L)
 Urinalysis: Inc. urine osmolality, inc. Na
d. Management:
 Correct underlying cause, if possible
 Monitor V/S, neuro, CV status
 Provide safe environment, particularly for the
client with LOC changes
 Restrict fluid intake (500 to 1000 mL/day)
 If fluid restriction is ineffective, give
DEMECLOCYCLINE (DECLOMYCIN) to
block the renal response to ADH and produce
water dieresis
 Furosemide (Lasix) with NSS or hypertonic saline
to maintain urine output and block ADH secretion
o 200 to 300 mL of 3% NSS slowly and
steadily increase Na; too rapid a rise may
cause cerebral edema
 MIO, vital signs, weight, watch out for
hyponatremia, serum and urine osmolality
V. THYROID GLAND
A. Hormones
1. Thyrocalcitonin or calcitonin – decreases serum calcium
level by transporting calcium from the blood to the bones
2. T3 – triiodothyronine; more active; for cellular
metabolism
3. T4 – tetraiodothyronine; thyroxine; for thermogenesis
** T3 and T4 are synthesized from Iodine and Tyrosine
B. Endocrine Disorders of the Thyroid gland
1. HYPOTHYROIDISM
a. Types:
 By age:
o Children: CRETINISM
o Adults: MYXEDEMA
 Location of dysfunction
o Primary or Thyroidal Hypothyroidism
- Problem on the thyroid gland itself
- Inc. TRH, inc. TSH, dec. T3 & T4
o Central Hypothyroidism
- Secondary or Pituitary
Hypothyroidism
 Inc. TRH, dec. TSH, dec. T3 &
T4
- Tertiary or Hypothalamic
Hypothyroidism
 Dec. TRH, dec. TSH, dec. T3 &
T4
b. Three basic concepts:
 Dec. T3 = dec. metabolic rate
 Dec. T4 = dec. body heat production
 Inc. calcitonin = inc. serum calcium level 
dec. neuromuscular activity
c. Assessment:
 Slowed physical and mental reactions
 Apathy, dull/expressionless/masklike face
 Generalized puffiness and edema around the eyes
and face (myxedema)
 Enlarged tongue, slow speech, husky or
hoarse voice
 Goiter may or may not be present
 Bradycardia, hyperlipidemia, atherosclerosis
  Anorexia, obesity, constipation, weight gain
 Irregular menstruation (menorrhagia,
amenorrhea)
 Cold intolerance; subnormal temperature; coarse,
dry, sparse hair; brittle nails, dry skin
 Extreme fatigue
 Hypoactive reflexes, weakness, muscle
aches, paresthesias
 Inc. sensitivity to ANTS (anesthetics/analgesics,
narcotics, tranquilizers, sedatives) = depressed
respi drive  alveolar hypoventilation 
progressive CO2 retention  narcosis, coma
(MYXEDEMA COMA)
d. MYXEDEMA COMA
 extreme severe stage of hypothyroidism
 characterized by HYPOTHERMIA &
UNCONSCIOUSNESS
 hypotension, bradycardia, hypothermia,
hyponatremia, hypoglycemia, generalized
edema, respiratory failure, coma
 precipitated by infection or other systemic
disease or by sedatives, opioid analgesics,
anesthetics, rapid withdrawal of thyroid
medication
 supportive care for myxedema coma
o ABG, pulse oximetry (hypercapnia,
hypoxia, metabolic acidosis)
o Assisted ventilation, oxygen; maintain
patent airway; aspiration precaution
o IV thyroid hormones (levothyroxine)
o IV fluids (NSS or hypertonic as
prescribed), glucose, corticosteroids
o Avoid hypnotics, sedatives, analgesics
o Keep patient warm
o Monitor temperature hourly, BP
frequently, changes in mental status,
electrolyte and glucose levels
e. Management:
 Orient patient to time, place, date, events
 Provide stimulation through conversation
 Explain meds:
o proloid (Thyroglobulin)
o dessicated thyroid extract
o cytomel (Liothyronine) – check BP, PR
before admin.; start with low dose and
gradually increase
o levothyroxine (Synthroid)
- increases blood glucose level
- watch out for ANGINA or
DYSRHYTHMIAS:
Hypothyroid patients have subnormal
metabolism and thus can tolerate a
reduction of blood supply and relatively
little O2. They are almost certain to
have increased cholesterol, CAD, and
atherosclerosis. Once levothyroxine
therapy is started, it increases O2
demand and enhances cardiovascular
effects of catecholamines
- instruct patient to report tachycardia,
chest pain, restlessness, nervousness,
insomnia, sweating, extreme weight
loss (signs of overdose or
hyperthyroidism)
- take the same time each day (AM)
without food
 monitor V/S, including heart rate and rhythm
 high fiber, low calorie, low fat diet
 increase fluids within restriction (give fluids
cautiously – may cause water intoxication)
 encourage mobility
 use laxatives and stool softeners sparingly
 encourage weight loss, weigh patient daily
 provide warm environment (extra blankets or
clothing; warm room)
 avoid exposure to cold and drafts
 monitor body temperature
 avoid external heat source (heating pads,
electric or warming blankets)
 space activities to promote rest and exercise as
tolerated
 assist in self-care activities when patient is
fatigued
 monitor patient’s response to increasing
activities
 Avoid sedatives and opioid analgesics
because of increased sensitivity to these
medications.
2. HYPERTHYROIDISM
a. GRAVE’S DISEASE is the most common cause of
hyperthyroidism
b. Three basic concepts:
 Inc. T3 = inc. metabolic rate
 Inc. T4 = inc. body heat production
 Inc. calcitonin = dec. serum calcium level 
inc. neuromuscular activity
c. Assessment:
 Irritability, agitation, mood swings, difficulty in
concentrating, nervousness, cannot sit or stand
still, hyperexcitable, apprehensive, fine tremors
of the hands
 Exophthalmus, corneal injury
 Goiter – enlargement of the thyroid gland
 Inc. PR, tachycardia, palpitations,
hypertension
 Diarrhea, inc. appetite, progressive weight
loss
 Amenorrhea
 Heat intolerance, fine tremors, shaky
handwriting, clumsiness
 Diaphoresis; warm, soft, moist skin; fine, silky
hairs, pliable nails
 Hyperactive reflexes
d. THYROID STORM
 stress, infection, surgery, manipulation of the
thyroid gland, overdose of thyroid medications
 ELEVATED TEMPERATURE (fever) – initial
sign
 Inc. BP, RR, CR; dysrhythmias, systolic
hypertension, nausea, vomiting, diarrhea, tremors,
anxiety, restlessness, agitation, confusion,
seizures, delirium, psychotic state, coma
 Thyroid storm management:
o Monitor V/S, MIO, neuro and CV status
o Maintain a patent airway and adequate
ventilation
o Administer PTU, Iodide, propranolol,
dexamethasone, glucocorticoids
o O2 as needed
o Maintain quiet, calm, cool, private
environment
o Lower fever (cooling devices, cold baths,
acetaminophen)
o Don’t use ASA – releases T3 & T4
e. Management:
 Provide rest, non-stimulating and cool
environment (no loud music, conversation, or
alarms)
 Promote safety
 Administer sedatives as ordered
 Avoid stimulants  THYROIDECTOMY
 Use calm, unhurried approach o Preop: maintain a EUTHYROID state
 Monitor level of consciousness - Administer iodides, antithyroid
 Suggest sunglasses to protect eyes from light agents, propranolol to prevent
 Frequently moisten the conjunctiva with eye thyroid storm
drops - ECG, V/S, weight, electrolytes,
 Improve self-esteem, address body image monitor for hyperglycemia
disturbance - Instruct on DBCT exercises
 Mirrors may be covered or removed o Postop:
 Avoid bringing physical changes to the - Monitor for respiratory distress
patient’s attention - SEMI-FOWLER’S with head, neck
 Avoid excessive palpation of the thyroid to and shoulder erect
prevent THYROID STORM - Watch out for complications:
 Monitor the ECG for arrhythmias  Hemorrhage – ice collar over
 Administer propranolol (Inderal) for the neck
tachycardia - Check dressing anteriorly
 High calorie, high protein diet and at the back of the neck
 Monitor weight of the patient  Airway obstruction – monitor for
 Balanced diet; small, frequent feedings (to 6x a respi distress (may be due to
day) laryngobronchospasm)
- Have tracheostomy set,
 Replace fluids lost through diarrhea and
O2, suction at bedside
diaphoresis
 Tetany (Hypocalcemia)
 Avoid highly seasoned foods and stimulants
- Monitor BP for
 A quiet environment during mealtime may aid Trousseau’s sign
digestion - Keep calcium gluconate
 Provide cool and quiet environment ready at bedside
 Cool baths, cool/cold drinks may provide  Recurrent laryngeal nerve
relief damage
 MIO, ensure adequate hydration and fluid - AEB respi obstruction,
balance dysphonia, high-pitched
 Promote safety and improve self-esteem voice, stridor, dysphagia,
 Drugs: restlessness
o Beta-blockers for tachycardia - Limit client talking
o Calcium-channel blockers - Ask patient to speak
o Dexamethasone – inhibits action of every hour
thyroid hormones  Thyroid storm
o Iodides: LUGOL’S SOLUTION (SSKI) - Monitor body temperature
- Decreases release of thyroid
hormones and the vascularity and VI. PARATHYROID GLANDS
size of the thyroid gland
- Used pre-thyroidectomy A. Hormone / function:
- Mix with fruit juice with ice or glass 1. Parathyroid hormone or parathormone or PTH – secreted in
of water response to decreased serum calcium level
- Provide drinking straw 2. PTH, therefore, increases serum calcium level by
- Side-effects: allergic reaction, transporting calcium from the bones to the blood
increased salivation
- Monitor for IODISM – vomiting, B. Endocrine disorders of the parathyroid glands:
abdominal pain, rash, sore gums and
salivary glands, metallic or brassy 1. HYPOPARATHYROIDISM
taste in the mouth a. Decreased secretion of PTH: HYPOCALCEMIA and
o Propylthiouracil (PTU) and methimazole HYPERPHOSPHATEMIA
(Tapazole) b. Assessment:
- Inhibits synthesis of thyroid  Latent signs and symptoms:
hormones o Numbness, tingling, cramps in the
- Do not interfere with release or extremities, stiffness of the hands and
activity of previously formed T3 & feet
T4  Overt signs and symptoms:
- Take with meals to avoid GI upset o Bronchospasm, laryngospasm,
- Side-effect: AGRANULOCYTOSIS carpopedal spasm, dysphagia,
(fever, sore throat, rashes) photophobia, cardiac dysrhythmias,
o Radioactive iodine therapy seizures
- Radioiodine is concentrated in the  Other signs and symptoms:
thyroid cells and destroys these cells o Anxiety, irritability, depression, delirium,
- Tasteless, colorless oral dose hypotension, ECG changes
- Body secretions will be radioactive; c. Management:
isolation for few days  Hypoparathyroidism after thyroidectomy:
- Not done to pregnant women; CALCIUM GLUCONATE
pregnancy delayed for 6 months o Caution in cardiac patients or those
after therapy taking digitalis
- Initially can cause an acute release of o If tetany and seizure activity do not subside
thyroid hormones: watch out for after calcium gluconate is taken,
THYROID STORM PENTOBARBITAL can be used
  Parenteral PTH only during acute episodes - Inform that talking may be painful
o Monitor for allergic reactions and serum for 1-2 days postop
calcium level o Postop – same with thyroidectomy
 Provide an environment free from noise,
drafts, bright lights or sudden movements; VII. ADRENAL GLANDS – aka SUPRARENAL GLANDS
SEIZURE PRECAUTIONS
 Watch out for RESPI DISTRESS A. ADRENAL CORTEX
o Have tracheostomy set, mechanical 1. Layers of the adrenal cortex:
ventilator, bronchodilators ready a. Zona glomerulosa
 Increase calcium and decrease phosphorus in b. Zona fasciculata
the diet c. Zona reticularis
o NO milk, milk products, and egg yolk – 2. Hormones of the adrenal cortex: STEROID
contain high level of P HORMONES
o NO spinach – contains OXALATE which a. ALDOSTERONE – produced by zona glomerulosa
would form insoluble calcium substances - Causes sodium and water retention (Salt)
 Supplement calcium in the diet b. GLUCOCORTICOIDS – produced by zona
 Amphojel to decrease P fasciculata
 Vitamin D preparations - Increases blood sugar level (Sugar)
 Wear Medic-Alert bracelet c. ANDROGENS – produced by zona reticularis
- Affects sex characteristics, personality and
2. HYPERPARATHYROIDISM mood (Sex)
a. Increased secretion of PTH: HYPERCALCEMIA and ***Aldosterone, glucocorticoids, and androgens help the
HYPOPHOSPHATEMIA body to adapt to all kinds of stress
b. Assessment: ***Without AGA, there will be circulatory shock and collapse
 May be asymptomatic ***main stimulus for aldosterone secretion: PRESENCE
 Irritability, neurosis to psychosis, apathy OF ANGIOTENSIN 2 IN THE BLOOD (RAAS)
 Hypertension, cardiac dysrhythmias ***minor stimulus for aldosterone secretion: ACTH
 Anorexia, nausea, vomiting, epigastric pain, ***main stimulus for glucocorticoid and androgen
constipation secretion: ACTH
 Fatigue, muscle weakness
 Bone decalcification (bone pain and B. ADRENAL MEDULLA
tenderness) 1. The middle or inner part of the adrenal glands
2. Part of the sympathetic nervous system
 Risk for fractures
3. Secretes catecholamines
 Risk for renal calculi
c. HYPERCALCEMIC CRISIS
C. Endocrine disorders of the Adrenal glands
 life-threatening neurologic, CV, and renal
symptoms
1. ADDISON’S DISEASE
 Management: IVF for rehydration, diuresis to a. Otherwise known as ADRENOCORTICAL
decrease calcium level, calcitonin + INSUFFICIENCY
corticosteroids, dialysis, pamidronate, etidronate b. Hyposecretion of AGA
(Didronel) c. Assessment:
d. Management:  Dec. Aldosterone:
 Education – may suspect as psychosomatic o Hyponatremia
 Hydration: o Water loss
o Increase oral fluid intake (greater than or o Hyperkalemia – muscle weakness and
equal to 2L/day) fatigue
o IV NSS o hypercalcemia
o MIO o Weight loss
o Cranberry juice to acidify urine o emaciation
o Prevent Dehydration (vomiting, diarrhea) to  Dec. Glucocorticoid:
avoid hypercalcemic crisis o Hypoglycemia
o No thiazide diuretics – decreased o Weakness, fatigue
excretion of calcium
o Mental status changes
 Monitor V/S, especially BP, cardiac o Anorexia
dysrhythmias o GI symptoms
 Monitor calcium and phosphorus levels  Dec. Androgens:
 Diet and medications: o Emotional lability
o Avoid diet with restricted or excess o Hair loss
calcium o Dec. hair growth
o Prune juice, stool softeners, physical o Menstrual changes in females
activity, inc. OFI o Impotence in males
o Oral phosphorus, calcitonin  Dark pigmentation of skin, knuckles, elbows,
 Mobility mucous membranes – due to inc. secretion of
o Move client slowly and carefully MSH
o Encourage walking or rocking chair  Inability to cope with stress – hypotension,
o NO BED REST – increased calcium risk for circulatory shock
excretion  renal calculi
d. ADDISONIAN / ADRENAL CRISIS
 Prepare and care for
 Due to overexertion, exposure to cold, acute
PARATHYROIDECTOMY
infections, dec. salt intake, stress of surgery,
o Preop – monitor electrolytes (Ca, P, Mg) dehydration from preop prep, abrupt withdrawal
- Ensure calcium levels are decreased
of steroid drugs
to near normal values
  Signs and symptoms of shock (dec. BP, inc. PR, o hypocalcemia
inc. RR)  Inc. Glucocorticoids:
 Cyanosis, pallor o Hyperglycemia
 Apprehension, confusion, restlessness o Protein catabolism
 Severe headache; severe abdominal, leg, and - Loss of muscle mass
lower back pain - Thin extremities
 Nausea, diarrhea, abdominal pain - Bleeding, ecchymosis
 Management: - Fragile skin - striae
o Restore blood circulation – MODIFIED  Inc. Androgens:
TRENDELENBURG POSITION o Virilization
o Maintain bed rest and provide a quiet o Hirsutism
environment o Breast atrophy
o Corticosteroids and fluids o Amenorrhea
- HYDROCORTISONE SODIUM o Clitoris enlargement
SUCCINATE (Solu-Cortef) IV, then o Voice deepening
followed by D5NS (glucose and o Loss of libido
sodium) o Gynecomastia
o Vasopressors o Mood swings
o Monitor V/S (BP), fluid status, neuro  Suppressed inflammatory response –
status increased susceptibility to infections
o Antibiotics c. Management:
e. Management:  Monitor V/S (BP), I&O, weight
 Monitor V/S (BP), weight, I&O  Monitor blood sugar level
 Monitor blood glucose and potassium level  MIO, weigh daily, monitor for edema
 CORTISONE or HYDROCORTISONE  Monitor WBC, Na, K, Ca
o A synthetic glucocorticoid  Observe hypertensive patients who also have
o Watch out for S/S of Cushing’s syndrome cardiac disease
(hyperglycemia, hypertension, weight gain,  Watch out for infections
etc.)
 High CHON, high K, low calories, low CHO,
o Decreases potassium; use K-sparing
low Na diet
diuretics to relieve water retention
 Careful passive ROM if with osteoporosis
o High K foods in the diet
 Balance rest and activity
o Decreases calcium – can lead to
osteoporosis  Provide meticulous skin care
o DON’T STOP ABRUPTLY – can lead to  Chemotherapy for inoperable adrenal tumors
ADDISONIAN CRISIS  Radiation if caused by pituitary adenoma
o An immunosuppressant – avoid  Prepare client for hypophysectomy
individuals with infections  Prepare client for adrenalectomy if caused by
o Causes GI irritation – administer after adrenal adenoma
meals or with antacids
 ORAL FLUDROCORTISONE (FLORINEF) 3. PRIMARY HYPERALDOSTERONISM /
o A synthetic mineralocorticoid CONN’S SYNDROME
o Prevents dangerous dehydration, a. Hypersecretion of aldosterone, usually caused by
hypotension, hyponatremia, adrenal tumor
hyperkalemia b. Assessment:
o Give High K foods as it decreases K  Hypernatremia
o Take with food or milk o Water retention
o Decreases K and Ca – hypernatremia, o Increased blood volume
water retention, osteoporosis, weight gain, o Hypertension
heart failure o Increased serum osmolality
o DO NOT STOP ABRUPTLY o polydipsia
 Client education:  Hypokalemia
o Avoid individuals with an infection o Headache, muscle weakness, cramping,
o High protein and high carbohydrate, fatigue
normal sodium intake in the diet o Inability of kidneys to concentrate or
o Avoid strenuous exercise and stressful acidify urine, polyuria, nocturia,
situations polydipsia, dec. urine specific gravity
o Avoid over-the-counter medications o Interference with insulin secretion from
o Wear a Medic-Alert bracelet pancreas, glucose intolerance
 Decreased hydrogen ions
2. CUSHING’S DISEASE and CUSHING’S SYNDROME o Increased blood pH and bicarbonate
a. Hypersecretion primarily of the glucocorticoids and o Metabolic alkalosis
androgen, although mineralocorticoids may also be  Hypokalemic alkalosis
increased o Hypocalcemia – tetany, paresthesias
b. Assessment:  Visual changes
 Inc. Aldosterone: c. Management:
o Hypernatremia  Monitor V/S (BP), hypokalemia,
o Water retention hypernatremia, I&O, urine specific gravity
o Weight gain  Spironolactone for hypertension
o Hypertension  K supplements
o Truncal obesity  Na restriction preoperatively
o Moon face  Adrenalectomy – hypokalemia resolves but
o Buffalo hump
hypertension may persist
o Hypokalemia
  Glucocorticoids preoperatively to prevent B. Endocrine function
adrenal hypofunction 1. The endocrine function of the pancreas is concentrated in the
 Monitor for adrenal insufficiency islets of Langerhans
postoperatively 2. The islets of Langerhans are composed of 3 major
 Instruct client regarding need for types of cells:
glucocorticoid therapy following a. Alpha cells – produces GLUCAGON (increases
adrenalectomy blood sugar level)
 Wear a Medic-Alert bracelet b. Beta cells – produces INSULIN (decreases blood sugar
level by transporting blood glucose into the cells to
4. PHEOCHROMOCYTOMA serve as cellular fuel or energy)
a. Catecholamine-releasing adrenal medullary tumor c. Delta cells – produces SOMATOSTATIN (regulates
b. Extra-adrenal tumor sites: blood sugar level by suppressing the release of
 Chest, Abdomen, Bladder, Brain glucagon and insulin from the islets)
c. Typically benign but can be malignant
d. Diagnosis: VANNILYLMANDELIC ACID (VMA) C. DIABETES MELLITUS (DM)
TEST 1. Diagnostic criteria:
 Avoid coffee, tea, cola, chocolate, bananas, a. FBS of > or equal to 126 mg/dL on 2 occasions
vanilla, aspirin b. RBS of > or equal to 200 mg/dL
 Specimen: 24-H urine collection c. 2° PPBS of > or equal to 200 mg/dL
 Normal: up to 14 mcg/100mL of urine 2. Types:
 (+) Pheochromocytoma: >14mcg/100mL of a. Type I DM
urine b. Type II DM
e. Assessment: c. GDM
 Triad of pheochromocytoma: d. Secondary DM
o Headache 3. TYPE I DM
o Diaphoresis a. Formerly known as INSULIN-DEPENDENT DM or
o Palpitations IDDM
 Tremors, flushing, anxiety, hyperglycemia b. Juvenile in onset
 Chest or abdominal pain with nausea and c. There is an absolute lack of insulin
vomiting d. Due to immunologic, genetic, and environmental
 Heat intolerance factors
e. Cells do not receive source of energy
 Weight loss
f. Cells use proteins and fats to yield glucose for
 5 H’s:
energy
o Hypertension
g. Usage of proteins cause muscles to be wasted and
o Headache
thinning of extremities and weight loss occur
o Hyperhidrosis
h. Usage of fats will yield fatty acids. Fatty acids
o Hypermetabolism
accumulate in the blood, leading to hyperlipidemia and
o hyperglycemia
ultimately atherosclerosis
f. Complications:
i. Additionally, fat breakdown (lipolysis) leads to the
 Acute renal failure
formation of KETONE BODIES (acetone, acetoacetic
 Cardiac dysrhythmias
acid, beta-hydroxybutyric acid)
 Aneurysms j. Ketone bodies are acidic and therefore can cause
 Stroke metabolic acidosis in the form of DIABETIC
g. Management: KETOACIDOSIS (DKA)
 Monitor V/S (BP, HR) k. DKA causes hyperventilation or KUSSMAUL’S
 Avoid increased abdominal pressure and RESPIRATIONS, and acetone breath
vigorous abdominal palpation 4. TYPE II DM
 Avoid smoking, drinking caffeine-containing a. Formerly known as NON-INSULIN DEPENDENT
beverages DM or NIDDM
 Bed rest with HOB elevated to promote b. Adult in onset
orthostatic decrease in BP, change position c. There is insulin resistance
slowly d. Due to obesity or lifestyle
 Provide nonstressful environment e. Cells may lack source of energy that is why the
 Monitor blood glucose level main problem is still hyperglycemia
 Provide a diet high in calories, vitamins, and f. Hyperglycemia increases the osmolality of the
minerals blood
g. No ketones are produced
 Alpha-1 blockers: phentolamine (Regitine) h. Can lead HHNS (HYPERGLYCEMIC
 Beta-blockers HYPEROSMOLAR NONKETOTIC SYNDROME)
 Smooth muscle relaxants: Na nitroprusside i. May be given Oral Hypoglycemic Agents (OHA)
(Nipride) j. Insulin may also be given – especially in times of
 Primary treatment is Adrenalectomy stress, surgery, illness, and pregnancy
5. Pathophysiologic changes
VIII.PANCREAS a. The main problem with DM is HYPERGLYCEMIA.
b. Hyperglycemia can lead to:
A. Exocrine function  Cellular starvation
1. Production and release of pancreatic enzymes to aid in o Polyphagia
digestion via the pancreatic duct into the duodenum: o May lead to CHON and fat breakdown
a. Amylase – digests carbohydrates o CHON breakdown leads to muscle
b. Trypsin – digests proteins wasting and weight loss
c. Lipase – digests fats o Fat breakdown leads to hyperlipidemia,
atherosclerosis and DKA
  Increased blood osmolality, which may o Check the expiration date on the test
cause: strips
o Increased blood viscosity o If the blood glucose level results do not
- Sluggish circulation seem reasonable, reread the instructions,
- Dec. tissue perfusion reassess technique, check the expiration date
- Proliferation of microbes of the test strips, and perform the procedure
- Degenerative or destructive again to verify results
changes (Complications of DM)  Urine testing for glucose – not a reliable
- Recurrent infections indicator of the blood glucose level and is
- Poor wound healing therefore no longer used for monitoring
o Increased osmotic pressure of the blood purposes
- Increased osmotic pull of fluid out of  Urine testing for ketones – should be performed
the ICF compartment during illness and whenever the client with
- Cellular dehydration
type 1 DM has persistently elevated blood
- Polydipsia
glucose levels (higher than 240 mg/dL for two
- Can lead to HHNS and HHNComa
consecutive testing periods)
(when brain cells are dehydrated,
 Glycosylated hemoglobin
LOC will decrease and coma may
o Blood glucose bound to hemoglobin
ensue)
o Determines patient’s compliance within the
 A glucose level that is more than the renal last 3 to 4 months of therapy.
threshold (normally 180-200 mg/dL only) o Fasting is not required
o Glucose may leak out into the urine: o Values are expressed as a percentage of
GLUCOSURIA / GLYCOSURIA the total hemoglobin
o Glycosuria increases the osmotic o Normal HbA1C for clients with DM is 4%
pressure of the urine to 6%
o Osmotic pull of glucose in the urine o The goal for clients with DM is HbA1c of
increases the fluid content of the urine: 7% or lower.
OSMOTIC DIURESIS o Elevated HbA1C means no compliance
o This can lead to Polyuria and ECF DHN d. Pharmacology
o Can lead to Polydipsia  Insulin
6. Management: NEMPE
o Rapid-acting insulin
a. Nutrition
- onset of action starts within 10 to 15
 Caloric distribution:
min after administration
o CHO = 50% to 60% - Advise client to eat within 10 to 15
o CHONS = 10% to 20% min after injection
o Fats = up to 30% Ex. Lispro (Humalog)
 Alcohol consumption o Short-acting insulin – CLEAR
o Take in moderation Ex. Regular insulin, semi-lente
o Can decrease blood glucose level o Intermediate-acting insulin – CLOUDY Ex.
o Take with food NPH (Neutral Protamine Hagedorn), lente
o Drink low-calorie or less sweet drinks o Long-acting insulin
(light beers or dry wine) Ex. Ultralente
 Sweeteners o Very-long acting insulin
o Take in moderation Ex. Lantus (Glargine)
o Nutritive sweeteners – provide calories o Onset, peak, and duration of short-
same with sucrose but less elevation in acting, intermediate-acting, and long-
blood sugar than sugar acting insulins
Ex. Fructose, sorbitol, xylitol Insulin Onset Peak Duration
***sorbitol has a laxative effect S ½-1H 2-4 H 6-8 H
o Non-nutritive sweeteners – provide I 1-2 H 6-8 H 16-24 H
minimal or no calories L 2-4 H 16-24H 32-36 H
Ex. Saccharin, aspartame, acesulfame- K, ***The peak action time of insulin is important
sucralose (Splenda) because of the possibility of hypoglycemic reactions
***sucralose (Splenda) is 600 times sweeter occurring during that time
than sugar  Oral Hypoglycemic Agents (OHA)
 Be wary of misleading food labels like  The following increases the
“sugarless”, “sugar-free”, “dietetic”, “health hypoglycemic effect of OHA:
food” - Aspirin
b. Exercise - Alcohol
 Initially can increase blood sugar level - Sulfonamides
 Net effect is lowering of blood sugar level - Oral contraceptives
 Do not exercise if blood glucose level is greater - MAOI
than 250mg/dL or urine tests positive for the  The following increases blood glucose
presence of ketones level while taking with OHA:
 Do not overexert or do unusual exercise - Glucocorticoids
c. Monitoring - Thiazide diuretics
 Self-monitoring of blood glucose (SMBG) - Estrogen
o Requires a finger prick to obtain a drop of o Sulfonylureas – stimulates the pancreas to
blood for testing release more insulin
o Wash hands before and after performing the - First-generation sulfonylureas:
procedure to prevent infection  Less expensive
o Follow the manufacturer’s instructions for
the glucometer
  More CV effects - Morning hyperglycemia
 Excreted only via the urine  Dawn phenomenon – normal
 Shorter duration of action than bld glucose until 3AM when
2nd generation sulfonylureas growth hormone rises; the effect
 Increased frequency of is increase in the bld glucose
administration level in the morning
 May lead to poor compliance  Insulin waning – progressive
Ex. chlorpropamide (Diabinese) rise in bld glucose level from
tolbutamide (Orinase) tolazamide bedtime to morning as insulin
(Tolinase) levels in the body gradually
- Second-generation sulfonylureas: decreases
 More expensive  Somogyi phenomenon – normal
 Less CV effects or elevated bld glucose level at
 Excreted via the urine and bile bedtime, a decrease at 2-3AM to
 Longer duration of action than 1st hypoglycemic levels; stress or
generation sulfonylureas counterregulatory hormones are
 Decreased frequency of released to compensate and the
administration effect is increase in the bld
 May lead to better compliance glucose level in the morning
Ex. glipizide (Glucatrol) - Hypoglycemia
glyburide (Micronase) glimepiride  Occurs when blood glucose level
(Amaryl) falls below 60 mg/dL or when the
o Meglitinides – stimulates the pancreas to blood glucose level drops rapidly
release more insulin from an elevated level
Ex. repaglinide (Prandin)  Mild hypoglycemia
o Biguanides – Major effect: decreases  Client remains fully awake
hepatic synthesis of glucose
but displays adrenergic
- Minor effect: increases peripheral symptoms; bld glucose level
uptake of glucose is usually lower than 60
Ex. metformin (Glucophage)
mg/dL
o Thiazolidinediones - Major effect:  Hunger, nervousness,
increases peripheral uptake of glucose
palpitations, sweating,
- Minor effect: decreases hepatic
tachycardia, tremor
synthesis of glucose
 Interventions:
Ex. rosiglitazone (Avandia)
 Give 10 to 15 g of a
pioglitazone (Actos)
fast-acting simple
o Alpha-glucosidase inhibitor – delays
carbohydrate (6-10
intestinal absorption of glucose
LifeSavers or hard
Ex. acarbose (Precose) miglitol
candies, 4-6 oz. of
(Glyset)
fruit juice or soda, 3- 4
e. Education
commercially prepared
 Insulin therapy
glucose tablets, 2-3
o Regular insulin is the only insulin that tsp. of sugar or honey)
can be administered intravenously
 Retest the blood
o The following increases the hypoglycemic
glucose level in 15
effect of insulin, causing a further decrease
mins and repeat the
in the blood glucose level:
treatment if
- Aspirin
symptoms do not
- Alcohol
resolve
- Oral anticoagulants
 Once the symptoms
- OHA
resolve, a snack
- Beta-blockers
containing protein and
- TCAs
carbohydrates, such as
- MAOIs
milk or cheese and
o The following increases the blood
glucose level: crackers, is
- Glucocorticoids recommended
- Thiazide diuretics unless the client plans
- Thyroid agents to eat a regular meal
- Oral contraceptives within 60 minutes
- Estrogen  Moderate hypoglycemia
 Client displays symptoms
o Illness, infection, and stress increase the
of worsening
blood glucose level and the need for insulin;
hypoglycemia; blood
insulin should not be withheld during illness,
infection, or stress because hyperglycemia glucose level is usually
and ketoacidosis can result lower than 40 mg/dL
 Confusion, double vision,
o Complications of insulin:
- Local and systemic allergic drowsiness, emotional
reactions changes, headache,
- Lipodystrophy (lipoatrophy and impaired coordination,
lipohypertrophy) inability to concentrate,
- Insulin resistance (due to obesity or
antibody production against insulin)
 irrational or combative
behavior, light- headedness,
numbness of the lips and
tongue, slurred speech
 Interventions:
 Administer 15 to 30 g
of a fast-acting simple
carbohydrate
 Administer additional
food such as low-fat
milk or cheese after 10
to 15 minutes
 Severe hypoglycemia
 Client displays severe
neuroglycopenic
symptoms; blood glucose
level is usually lower than
20 mg/dL
 Difficulty arousing,
disoriented behavior, loss of
consciousness, seizures
 Interventions:
 Notify the physician
 If the client is
unconscious and
cannot swallow, an
injection of glucagon 1
mg is administered SC
or IM
 Administer a second
dose in 10 mins if the
client remains
unconscious
 Small meal is given
when client awakens
as long as he is not
nauseated
 In the hospital or ER,
the client may be
treated with an IV
injection of 25 to 50
mL of D50W
o Alternative methods of insulin delivery
- Insulin pens and disposable
needles
 Using an prefilled insulin
cartridge
- Jet injectors
 Delivers insulin through the
skin under pressure in an
extremely fine stream
 Bruising has occurred in some
patients
- Insulin pumps
 3mL syringe attached to a 24- to
42-inch tube
 Needle/catheter is inserted to
subcutaneous layer and secured
with tapes
 Change needle/catheter at
least every 3 days
 Pump worn on belt, pocket or
bra
 Provides a continuous basal
rate and the client delivers a
bolus rate of insulin before
each meal
 lispro (Humalog) and regular
insulin are appropriate for use in
these pumps
- Implantable insulin delivery
 An insulin pump is implanted in
the peritoneal cavity, where
insulin can be absorbed in a
more physiological manner
- Inhalant and transdermal (patch) insulin
delivery – under research
o Storage
- Vial not in use: refrigerated
- Vial in use: room temperature to
reduce local irritation at injection
site
- Spare vials are considered vials not in
use
- Avoid extremes of temperature
o Cloudy insulin must be thoroughly mixed by
gently inverting the vial or rolling in between
palms of the hands before drawing
o Mixing insulin into a syringe
- Injecting air into the vial:
 Inject air into the vial of the
cloudy insulin first, then into
the vial of the clear insulin
 Not withdrawing the syringe
from the vial of the clear insulin,
gently invert the vial of the clear
insulin
- Withdrawing or aspirating the
insulin:
 Withdraw or aspirate from the
vial of the clear insulin first,
followed by the vial of the
cloudy insulin
- An easy way to remember this is
through the mnemonic NR-RN
(inject air into NPH [cloudy] first
then into the Regular [clear];
withdraw/aspirate Regular [clear]
first then the NPH [cloudy])
o Rotate injection sites within 1 anatomic
site at a time
- Anatomic sites: abdomen, posterior
aspect of the upper arms, hips, upper
thighs
- Distance bet injection sites is 0.5 to 1
inch
o Cleansing injection site with alcohol is not a
must. If alcohol was used to cleanse injection
site, let the applied alcohol dry first to
prevent seepage of the alcohol into the
injection site causing local irritation
o Do not aspirate for blood
 Pancreas transplantation are performed on a
limited number of clients (generally, these are
clients who are undergoing kidney transplantation
simultaneously); immunosuppressive therapy is
prescribed to prevent and treat rejection
 Complications
o Acute complications:
- Diabetic Ketoacidosis (DKA)
 Sudden in onset
 Precipitated by infection,
stress, inadequate insulin
dose
 Assessment:
 Hyperglycemia
 Dehydration: polyuria,
polydipsia, weight loss,
dry skin, sunken eyes,
soft eyeballs, lethargy,
coma
 Ketosis: kussmaul’s
respiration,
“fruity”/acetone breath,
nausea, abdominal pain
  Acidosis
 Interventions:
 Restore circulating blood
volume and protect against
cerebral, coronary, or renal
hypoperfusion
 Rapid IV infusions of
0.9% or 0.45% NS
 D5NS or 5% dextrose in
0.45% saline when the
blood glucose level
reaches 250 to 300 mg/dL
 Administer IV regular
insulin
 Monitor for potassium,
glucose levels and for
signs of increased ICP
during insulin therapy
 If blood glucose level falls
too far or too fast before the
brain has to time to
equilibrate, water is pulled
from the blood to the CSF
and the brain, causing
cerebral edema and
increased ICP
 K IV in a diluted solution as
prescribed when K reaches
a normal level to prevent
hypokalemia
 Ensure adequate renal
function before
administering potassium
- Hyperglycemic Hyperosmolar
Non-Ketotic Syndrome (HHNS)
 Gradual in onset
 Precipitated by infection,
stress, and poor fluid intake
 Assessment:
 Major difference with
DKA is that ketosis and
acidosis do not occur
 Altered CNS function with
neurologic symptoms
 Dehydration: polyuria,
polydipsia, weight loss,
dry skin, sunken eyes,
soft eyeballs, lethargy,
coma
 Interventions:
 Treatment is similar to
that for DKA
 Fluid replacement,
correction of electrolyte
imbalances, insulin
administration
 Insulin plays a less critical
role in the treatment of
HHNS than it does for the
treatment for DKA because
ketosis and acidosis do not
occur; rehydration alone
may decrease glucose levels
o Chronic complications:
- Microvascular complications:
 Diabetic retinopathy
 Description:
 Chronic and
progressive
impairment of the
retinal circulation
that eventually causes
hemorrhage
 Permanent vision
changes and blindness
can occur
 The client has
difficulty with
carrying out the daily
tasks of blood glucose
testing and insulin
injections
 Assessment:
 A change in vision is
caused by the rupture
of small
microaneurysms in
retinal blood vessels
 Blurred vision results
from macular edema
 Sudden loss of
vision results from
retinal detachment
 Cataracts result from
lens opacity
 Interventions:
 Maintain safety
 Prevention by control
of HPN and blood
glucose levels
 Photocoagulation
(laser therapy)
removes hemorrhagic
tissue to decrease
scarring and prevent
progression of the
disease process
 Vitrectomy removes
vitreous
hemorrhages and thus
decreases tension on
the retina, preventing
detachment
 Cataract removal
with lens
implantation
improves vision
 Diabetic nephropathy
 Description:
 Progressive
decrease in kidney
function
 Assessment:
 Microalbuminuria
 Thirst
 Fatigue
 Anemia
 Weight loss
 Sings of malnutrition
 Frequent UTIs
 Sings of neurogenic
bladder
 Interventions:
 Prevention by control
of HPN and blood
glucose levels
 Assess V/S, monitor
I&O, serum BUN and
crea, and urine
albumin levels
 Restrict dietary
protein, sodium, and
potassium intake as
prescribed
  Avoid nephrotoxic intercourse (female)
drugs  Assessment:
 Prepare for dialysis,  Paresthesias
kidney transplant,  Decreased or absent
pancreas transplant as reflexes
prescribed  Decreased
 Neuropathy sensation to
 Description: vibration or light
 General deterioration touch
of the nervous system  Pain, aching, and
throughout the body burning in the lower
 Complications extremities
include the  Poor peripheral
development of pulses
nonhealing ulcers of  Skin breakdown and
the feet, gastric signs of infection
paresis, and erectile  Weakness or loss of
dysfunction sensation in cranial
 Classifications: nerves III, IV, V, and
 Focal neuropathy or VI
mononeuropathy –  Dizziness and postural
involves a single hypotension
nerve or group of  Nausea and
nerves, most vomiting
frequently cranial  Diarrhea or
nerves III and VI, constipation
resulting in diplopia;  Incontinence
usually resolves  Dyspareunia
spontaneously  Impotence
 Sensory or  Hypoglycemic
peripheral unawareness
neuropathy – affects  Interventions:
distal portion of  Prevention is by
nerves, most control of HPN and
frequently in the lower blood glucose levels
extremities  Administer pain
 Autonomic medications as
neuropathy – prescribed
symptoms vary  Estrogen-containing
according to organ lubricants for women
system involved with dyspareunia
 Cardiovascular  Careful foot care
– cardiac  Inspect the feet
denervation daily
syndrome (heart  Wash with
rate does not warm water and
respond to mild soap
changes in  Pat them dry –
oxygenation do not rub
needs) and  Wear
orthostatic comfortable,
hypotension properly-fitted
occur pair of shoes
 Pupillary – pupil  Use white
does not dilate in cotton socks
response to  Do not go
decreased light barefooted
 Gastric –  Trim toenails
decreased straight across
gastric  Do not cut the
emptying lateral edges –
(gastroparesis) ingrown may
 Urinary – develop
neurogenic  Exercise or
bladder massage the
 Sudomotor: feet
decreased  Do not wear
sweating knee-high or
 Adrenal – stay-up
hypoglycemic stockings
unawareness  Consult a
 Reproductive – Podiatrist for
impotence any injury
(male), painful
 - Macrovascular complications:
 Cerebrovascular diseases
 TIAs
 Stroke
 Cardiovascular diseases
 MI, usually silent due to
accompanying autonomic
neuropathy
 CAD
 Peripheral vascular diseases
 PAOD
 PVOD
 Management:
 Prevention and treatment of
atherosclerosis
 Diet and exercise to
manage obesity, HPN,
and hyperlipidemia
 Smoking cessation
 Control of blood glucose
levels
 Insulin
 May need to be
increased during
illnesses
 Client may need to
switch from OHA to
insulin during
illnesses

RESOURCES:

1. Brunner & Suddarth’s Textbook of Medical-Surgical Nursing, 10th edition, Volume 2

2. Saunders’s Comprehensive Review for the NCLEX-RN Examination, 4th edition
3. Straight A’s in Pathophysiology by Lippincott Williams & Wilkins
4. Straight A’s in Anatomy & Physiology by Lippincott Williams & Wilkins
5. Medical-Surgical Nursing: Concepts and Clinical Application, 1st edition by Josie Quiambao-Udan, RN, MAN