2023 Med Surg

COPYRIGHT: JONAS MARVIN M.
ANAQUE, RM, RN
MEDICAL SURGICAL NURSING | ENDOCRINE DISORDERS

Endocrinology — study of the structures and functions of the endocrine system
Endocrinologist — medical doctor who specializes in the diagnosis and treatment of endocrine
diseases and disorders
Endocrine gland is a gland whose secretions (called hormones) are collected by the blood and
reach the tissues through the circulation.
Major glands of the endocrine system includes:
Pineal gland
Pituitary gland
Thyroid gland
Parathyroid gland
Adrenal glands
Pancreatic islets
Ovaries
Testes
Hypothalamus.
The hypothalamus and pituitary gland are neuroendocrine organs.
Endocrine Versus Exocrine gland

Exocrine glands secrete hormones into ducts.
Endocrine glands secrete hormones directly into the blood stream.
Hypothalamus — Master control center of the endocrine system, located in the brain.
 It works to maintain homeostasis, coordinates nervous and endocrine systems
 Hypothalamus is the heart of the endocrine system, maintains homeostasis
 Endocrine system and hypothalamus are interrelated
 HYPOTHALAMUS is link between the nervous system and the endocrine system
 Uses the pituitary gland to link the nervous system to the endocrine system
Hormones — chemical released into the blood stream directly onto a target cell.
UNIQUE CHARACTERISTIC: Influence cellular activity of specific target tissues
hormone is an "intercellular signal" — chemical substance, a molecule that is secreted by one

cell of the body and modifies the function of another cell of the body.
All cells in the body are believed to have intracellular receptors for Thyroid hormone
kind of cells can be a source of hormones: Neurons, neurohormones, endocrine cells, immune
cells
 Epinephrine (monoamine) example of a molecule that is utilized in the body as both a
hormone and a neurotransmitter.
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COPYRIGHT: JONAS MARVIN M. ANAQUE, RM, RN
PITUITARY DISORDERS
Pituitary gland— a pea-sized gland, known as the MASTER GLAND

1. Gigantism/Acromegaly
Gigantism – children
Acromegaly – adults
Acromegaly – condition brought about by overproduction of growth hormone by the pituitary
gland in Adults.
Acromegaly, which is caused by a pituitary tumor that releases excessive growth hormone, is
associated with hyperglycemia, hypertension, diaphoresis, peripheral neuropathy, and
joint pain
Cause: adenoma – noncancerous (benign) pituitary tumor.
Non pituitary tumors: pancreas and lungs
S/sx onset: 20-40 years old

Hallmark: coarse facial features.
Signs and symptoms:

L – Lantern jaw (prognathism)
A – abnormally large hands and feet
R – requires larger rings, shirts, shoe size increase
G – gaps and misalignment of teeth
E – enlargement of hands feet, skull , tongue, nose, lips
J – joint paint (arthritis) , weakness and severe headache

A – deepened, husky voice
W – with visual, menstrual, erectile dysfunction problems
First nursing diagnosis: Risk for Trauma /injury (arthritis and falls)
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Best time to buy shoes: late afternoon/evening.
Diagnostic test:
1. Screening
Insulin-like growth factor 1 (IGF-1)
Most relevant test due to steady secretion
Highly specific if elevated
2. Growth hormone suppression test.– best method to confirm acromegaly.

 Perform glucose tolerance test (GTT) and measure GH
 Administer 75 g glucose and perform GH measurements over 120 minutes
 Failure to suppress GH during hyperglycemia is diagnostic
 GH <1 ng/mL excludes acromegaly
3. CT scan and MRI — to look for abnormal growths in the pituitary gland.
Treatment: combination of surgery, radiation, and drug therapy

Surgery – first choice in pituitary tumors (adenoma)
 Transsphenoidal hypophysectomy — involves entry into the sella turcica through an
incision in the upper lip and gingiva into the floor of the nose and the sphenoid
sinuses.
 Removal of Pituitary gland through nasal passage.
After surgery: Assessment of AIRWAY is priority.

Check Rhinorrhea: check nasal discharges for halo sign and glucose maybe a sign of CSF
leakage
 Call doctor of halo sign is present on the nasal dressing, indicates cerebrospinal fluid.
halo sign-- blood in the middle and yellow in surrounding or clear with yellow color at the
edge.
 glucose level greater than 30 mg/dL indicates a CSF leak
Risk for meningitis – assess for severe headache, fever, and nuchal rigidity
Serious complication of hypophysectomy: transient Diabetes Insipidus; check POLYURIA
Drug of choice: Parlodel

 Octreotide (somatostatin analog)
 Cabergoline (dopamine agonist)
 Pegvisomant (GH receptor antagonist)
 Avoid somatropin (Genotropin) drug
Complications: Cardiomegaly, Heart failure, DM, HTN

 higher risk for colon polyps and colorectal cancer, and should have a screening
colonoscopy performed every three to four years
NURSING INTERVENTION
1. MOST important nursing intervention monitor the pupillary response, speech
patterns, and extremity strength to detect neurologic complications.
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2. head of the bed is elevated at all times to a 30-degree angle to avoid pressure on the
sella turcica and to decrease headaches, a frequent postoperative problem.
3. Perform mouth care for the patient every four hours to keep the surgical area clean and
free of debris.
4. Notify the surgeon and send any clear nasal fluid to the laboratory to test for glucose.
5. Tooth brushing should be avoided for 10 days to protect the suture line.
6. Vigorous coughing and sneezing should be avoided to prevent cerebrospinal
leakage.
7. A severe headache may indicate cerebrospinal leakage into the sinuses.
8. Straining with bowel movements may cause cerebrospinal leakage.
9. postnasal drip or increased swallowing after surgery indicates CSF leakage
2. Gigantism — condition brought about by overproduction of growth hormone by the

pituitary gland in children. Observe for Hyperglycemia.
More common in males
Cause: adenoma, a tumor of the pituitary gland.

 Hypersecretion of growth hormone (GH) before normal bone growth has stopped.
ONSET: before the end of puberty, Originates during infancy as early as the first 6 to 9
months of age.
 Usually GH affects LOWER LIMBS
Symptom of gigantism is characterized by: Weakness
SIGNS AND SYMPTOMS
G – gaps between teeth, prominent forehead and jaw

I – irregular menstruation, delayed puberty, lactation
A – abnormally tall stature.
N – noticeable enlargement of hands & thick feet, fingers and toes
T – thickening of facial features
S – sleep disorders, Double vision, headache, and deafness
Management:
1. Surgery
Hypophysectomy: Removal of a pituitary tumor via endoscopic transnasal (most
common) or craniotomy
2. Radiation Therapy
o Shrinks pituitary tumor over a period of time (5-10 years).
3. Medication
 Somatostatin analogs (inhibit the release of growth hormone)
Craniotomy complications:
1. intercranial pressure (ICP)
2. Bleeding
3. Menigitis
4. Hypopituitarism
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3. GALACTORRHEA production of breast milk in men or in women who are NOT

breastfeeding.
CAUSE: Pituitary tumor (prolactinoma)– overproduction of the hormone prolactin

PROLACTINOMA – is the most common pituitary tumor
Prolactin is a hormone that stimulates the breasts to produce milk.
Hallmark: unexpected breast milk production
Signs and Symptoms

D – dryness of vagina causing dyspareunia
E – erectile dysfunction and reduced libido
D – disrupted menstrual flow or amenorrhea
E – excessive hair growth (hirsutism)
Diagnosis:
 Measurement of blood prolactin level
 CT Scan or MRI
Lab results:
Male: low testosterone level
Female: low estrogen, high prolactin
Low estrogen in women and low testosterone in men INCREASES the RISK FOR
OSTEOPOROSIS
**Infertility is common
COLLABORATIVE approach: Endocrinologist and Ophthalmologist for visual problems

Treatment:
1st: dopamine agonist (cabergoline, bromocriptine, pergolide)
 bromocriptine and cabergoline (3yrs therapy)— it mimics dopamine to block prolactin
2nd: surgery
THYROID GLAND
Shape: butterfly
ASSESSMENT TOOL: PALPATION
 To palpate the thyroid, use a posterior approach.
 Stand behind the client and ask the client to lower the chin to the chest and turn the neck
slightly to the right.
 To inspect movement of the client's thyroid gland, the nurse should ask the client to
SWALLOW A SMALL SIP OF WATER
Location: located inferior to the larynx and anterior to the trachea just below the thyroid
cartilage (Adam's apple)
Thyroid Hormones:
1. Triiodothyronine (T3) – controls energy levels, temperature, metabolism, heart rate,
blood pressure and development of a fetus
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2. thyroxine (T4)— controls how the heart works, metabolism, health of the muscles and
bones and brain development.
3. Calcitonin- controls the amount of calcium and phosphate in the blood
TAKE NOTE: TSH is NOT produce by thyroid gland
APG — produces TSH (thyroid stimulating hormone) and stimulates T3 and T4 production
EUTHYROIDISM — Normal functioning of thyroid gland
Three types of thyroid disorders:

Hyperthyroidism — LOW TSH, HIGH T3&T4
Hypothyroidism— HIGH TSH, LOW T3&T4
Goiter — nutritional deficiency of IODINE
THYROID DISORDERS
1. Hyperthyroidism – Hyperthyroidism is the overactivity of the thyroid gland
ASSESSMENT TOOLS:
Palpation — for thyroid enlargement
Auscultation — for BRUIT sound
 A bruit is a soft, swishing sound produced because of an increase in blood flow
through the thyroid arteries
Hyperthyroidism Cause: LOW in TSH , HIGH in T3 and T4
Primary disease: Grave's disease (most common cause)

Secondary disease: Inappropriate TSH secretion
Hyperthyroidism causes
 GRAVES disease – MOST COMMON CAUSE, autoimmune
 excess secretion of TSH by pituitary gland
 Thyroiditis: inflammation of thyroid gland causes thyroid hormone to leak into blood
 neoplasms (toxic multinodular goiter) — not autoimmune cause
 excessive intake of thyroid medication
Hyperthyroidism risk factors

 10x more common in women than men
 Genetics
 increased iodine intake
 age between 20-40 years
Graves disease (hyperthyroidism with toxic goiter)

 most common cause of hyperthyroidism (overactivity of thyroid gland)
 an autoimmune disorder sometimes associated with other autoimmune disorders such
as myasthenia graves and pernicious anemia
 clients with this have a antibody in their serum that binds to TSH receptors in the thyroid
follicles and causes the thyroid cells to hyper function
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 when the antibody binds to TSH receptors on the thyroid gland it stimulates hormone
synthesis and secretion which enlarges the gland (GOITER)
Hallmark sign: Exophthalmos or proptosis (protrusion; bulging outward) and visual
dysfunction
 blurred vision, diplopia, eye pain, lacrimation, and photophobia
 heat intolerance, increased energy, difficulty sleeping, diarrhea, and anxiety.
 inability to close eye lids completely increased risk for corneal dryness, irritation, risk for
infection, and ulceration – USE ARTIFICIAL TEARS
 Infiltration of the muscles that move the eye and of the optic nerve leads to paralysis and
vision loss
HYPERTHYROIDISM Hallmark Sign: Poor Thermoregulation and Heat intolerance
HYPERTHYROIDISM Signs and Symptoms:

H – heat intolerance
Y – Yucky diarrhea (increased peristalsis, bloating, and pain),
P – Palpitations and tachycardia
E – Exophthalmos with Graves disease
R – restless, irritable, and fatigue
T – Tremors (fine hands tremors or fine fingers tremors)
H – hair loss in the scalp, axillary, eye brow, or pubic areas or Fine straight hair
Y – Yucky skin, excessive sweating (diaphoresis)
R – retraction of Eyelids (globe lag or Von Graefe's sign)
O – Older patients may develop cardiac dysrhythmias (A-fib)
I – increased appetite but loses weight (WEIGHT LOSS)
D – DTR is hyperactive with Muscle weakness
I – Insomnia and increased libido
S – smooth, warm, moist skin
M – muscle wasting and menstrual changes (Amenorrhea)
Personality changes: moody, manic, Emotional lability, decrease attention span

Eye changes: Blurred or double vision, Eye fatigue, Corneal ulcers or infections, increased
tears, red conjunctiva or blood shot eyes, Photophobia
Other Manifestations
• Goiter
• Wide-eyed or startled appearance (exophthalmos)
• Decreased total white blood cell count
• Enlarged spleen
Hyperthyroidism Nursing Diagnosis:

1. Risk for increased cardiac output
2. Imbalanced Nutrition
3. Disturbed Sensory perception
4. Disturbed Body Image
HIGHEST PRIORITY NURSING DIAGNOSIS: Imbalanced nutrition: LESS than body

requirements related to thyroid hormone excess
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Hyperthyroidism Diagnostic tests

1. Thyroid antibodies (TA) test: elevated in graves disease
2. TSH test (sensitive assay): Serum TSH are measured and compared to T4 levels to
differentiate pituitary from thyroid dysfunction; decreased in primary hyperthyroidism
-T4 test: increased levels of T4
-T3 test: increased levels of T3
-T3 uptake: Increased
3. RAI uptake test: increased uptake seen in graves
-Thyroid suppression: Increased RAI uptake and T4 levels
4. thyroid scan - evaluates the position, size, and functioning of the thyroid gland.
 Pregnancy should be ruled out before the scan is performed.
Hyperthyroid labs: decreased TSH, increased T3 and T4
Hyperthyroidism Medications
Propylthiouracil (PTU), Methimazole, Iodine, Beta Blockers, Ca channel blockers, Radioactive
sodium iodine, surgery
Drug of Choice: Propylthiouracil-PTU

Indication: Blocks production of thyroid hormone and prevents conversion of T3 and T4 at
cellular level.
Dosage: 300-900mg/day PO in adults
Doses: 3 doses (every 8hours) , 2 doses (every 12 hours)
Duration: 6 mos - 2 years or 12 to 18 months
How long may it take to produce a euthyroid effect: 3-12 weeks
Priority to MONITOR: CBC laboratory test
Thyroid function tests: performed every 4-6 weeks
DIET: High calorie, high protein diet, high carbohydrates
Drug Interactions
1. Anticoagulants - Increased risk of bleeding
2. Iodine-containing foods/supplements and Thyroid Agents antagonizes effects
3. Cross-sensitivity with Methimazole
4. Dixogin - Increased glycoside effects
Treatment of Overdose
 A thyroid agent to correct hypothyroidism
 Atropine for bradycardia
 Gastric Lavage
 Sodium Thiosulfate
Adverse side effects are:

A – agranulocytosis and aplastic anemia
N – Nausea and vomiting and DROWSINESS
T – thrombocytopenia and leukopenia
I – increased BUN & creatinine levels
T – toxicity in liver and bone marrow
H – hepatitis
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Y – you may loss taste

R – Rashes
O – output of urine decreases
I – increase risk of nephritis
D – diarrhea
Most serious toxicity of PTU: Agranulocytosis (usually during first 2 months of Tx)
Monitor the patient for: Fever, Chills, malaise and sore throat (coughing)
Monitor: BLOOD TEST (CBC)
Nursing Implications
- Take medication at same time each day
- Give with meals to reduce GI distress
- Advise patient that effects can take 3-12 weeks for effects
- Monitor VS, Weight, I/O
- NEVER stop taking abruptly ( thyroid crisis can occur)
- Monitor for S/S of hyperthyroidism
- Monitor for S/S of hypothyroidism
- Do not take OTC without talking to HCP
- Monitor CBC for leukopenia
- avoid iodine rich foods
- NO to ASPIRIN drug
- Monitor for adverse effects
Others: methimazole 15-60mg/day PO – fewer side effects, treatment of graves disease, do

not give in 1st trimester
Methimazole is an iodine preparation that decreases blood flow through the thyroid gland.
Beta blockers (propanolol, inderal) -treat high blood pressure, reduce a rapid heart rate and
help prevent palpitations.
Radioactive Iodine Therapy

RAIU – Sodium iodide 131I (Iodotope) is a radioactive isotope of iodine
Administered by mouth (P.O)
The half-life of 123I is short, and radiation precautions are not needed.
The normal thyroid gland has an uptake of 5% to 35% of the given dose at 24 hours. RAIU is
increased in hyperthyroidism.
 Radioactive iodine, causes the gland to SHRINK and symptoms to subside, usually
within three to six months
 thyroid gland takes up iodine in any form, RAIU damages or destroys thyroid cells so
they produce less TH
 results in 6-8 weeks
 contraindicated in pregnant and lactating women, can cross placenta and damages
fetal thyroid gland
 metallic taste and burning sensation in the mouth, sore teeth and gums, diarrhea;
staining of teeth, skin rash, and development of goiter
 only for patients over 30 years old because of adverse effects associated with
radioactivity.
 Give iodine solution through a straw to decrease staining of teeth; tablets can be
crushed.
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RAI
RAI therapy is performed on an outpatient basis.
 The radiation dose is low and is usually completely eliminated within a month
 In unsealed RAI, some radioactivity is present in the patient's body fluids and stool for a
few weeks after therapy.
 Radiation precautions are needed to prevent exposure to family members and other
people.
The degree of thyroid destruction varies. Some patients become hypothyroid as a result
of treatment
Safety Precautions for the Patient Receiving an Unsealed Radioactive Isotope

• Use a toilet that is not used by others for least 2 weeks after receiving the radioactive
iodine.
• Sit to urinate (males and females) to avoid splashing the seat, walls, and floor.
• Flush the toilet three times after each use.
• If urine is spilled on the toilet seat or floor, use paper tissues or towels to clean it up, bag them
in sealable plastic bags, and take them to the hospital's radiation therapy department.
• Men with urinary incontinence should use condom catheters and a drainage bag rather than
absorbent gel-filled briefs or pads.
• Women with urinary incontinence should use facial tissue layers in their clothing to catch the
urine rather than absorbent gel-filled briefs or pads.
• Using a laxative on the second and third days after receiving the radioactive drug helps you
excrete the contaminated stool faster (this also decreases the exposure of your abdominal
organs to radiation).
• Wear only machine-washable clothing, and wash these items separate from others in your
household.
• After washing your clothing, run the washing machine for a full cycle on empty before it is used
to wash the clothing of others.
• Avoid close contact with pregnant women, infants, and young children for the first week
after therapy. Remain at least 3 feet (about 1 meter) away from these people, and limit your
exposure to them to no more than 1 hour daily.
• Some radioactivity will be in your saliva during the first week after therapy. Precautions to
avoid exposing others to this contamination (both household members and trash collectors)
include:
•Not sharing toothbrushes or toothpaste tubes
•Using disposable tissues, rather than cloth handkerchiefs, and either flushing used ones
down the toilet or keeping them in a plastic bag and turning them in to the radiation department
of the hospital for disposal
•Use disposable utensils, plates, and cups
•Selecting foods that can be eaten completely and do not result in a saliva-coated remnant
(Foods to avoid are fruit with a core that can be contaminated, meat with a bone [e.g., chicken
wings or legs, ribs])
Surgery
-Some clients have such an enlarged thyroid gland that pressure on the esophagus or trachea
cause problems with breathing or swallowing.
---subtotal thyroidectomy
---total thyroidectomy
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-PREOP:
-before this the patient should be as close to euthyroid state as possible
-may be given antithyroid drugs or iodine preparations to decrease vascularity and size of gland
PreOp drug: Saturated solution of potassium iodide (SSKI)

an iodine preparation used to treat hyperthyroidism.
• Drug inhibit release of thyroid hormones, causing them to accumulate in the thyroid gland.
• Used to decrease the size and vascularity of the thyroid gland before thyroidectomy.
• SSKI is more often used as an expectorant
---> also decrease risk of hemorrhage during and after surgery
Subtotal thyroidectomy
-usually is performed
-they leave in enough to produce an adequate amount of TH
Total thyroidectomy
-performed to treat cancer of the thyroid
-requires lifelong hormone replacement
Postop care of subtotal thyroidectomy

 Monitor vital signs every 15 minutes until the patient is stable and then every 30 minutes
for 24 hours.
IMPORTANT INTERVENTIONS: coughing (deep breathing), splinting wound, respiratory

distress, trach kit, O2, suction and semi-fowlers position
POST OP POSITION: SEMI FOWLERS

- -support head and neck with sandbags or pillows
To avoid pressure on the suture line, encourage the client to avoid neck flexion or extension
Maintain the bed in a high-Flower's position to decrease edema and swelling of the neck.
PRIORITY ASSESSMENTS
1. Hemorrhage
 greatest in first 12 to 24 hours after, assess dressing for drainage
 Serosanguinous drainage is NORMAL – PINKISH RED
 Check the client's dressing and palpate the back of the neck, where drainage tends to
flow. Expect about 50 mL of drainage in the first 24 hr.
 If you find no drainage, check for drain kinking or the need to reestablish suction.
 Expect only scant drainage after 24 hr.
monitor BP and pulse for signs of hypovolemic shock
2. Respiratory distress
 assess Respiratory rate, rhythm, depth, and effort
 Assess for dyspnea, stridor, "crowing," and cyanosis. Note quality of voice.
 humidification as ordered, Humidifying the air promotes easier respiration and thins
respiratory secretions.
assist with coughing and deep breathing every 30 minutes to 1 hour.
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 have suction, oxygen, and a tracheostomy set available within 24 hours
3. laryngeal nerve damage

 Check for laryngeal nerve damage by asking the client to speak as soon as she
awakens
 assess ability to speak, noting quality and tone
 hoarseness and a weak voice (whispery voice) is transient and NORMAL
4. Tetany (hypocalcemia)
 assess for signs of calcium deficiency: tingling of toes, fingers, and lips, muscular
twitches; positive chvosteks sign and trousseaus sign; decreased serum calcium
levels
 keep calcium gluconate or calcium chloride IV available for immediate use
 Hypocalcemia with tetany (usually transient) may occur 1-7 days postoperatively
and indicates hypoparathyroidism, which can occur as a result of inadvertent
trauma to/partial-to-total removal of parathyroid gland(s) during surgery.
 Semi fowlers, assess for Chvostek (face spasm when touch cheek) & Trousseau
sign(pump up BP cuff & hand curls).
WOF: Thyroid storm or thyrotoxicosis

Thyroid Storm – Life-threatening complication for hyperthryoidism
Common Cause: untreated hyperthyroidism (most often graves disease)
And NOT taking antithyroid medications properly.
Predisposing factors: individuals w/ hyperthyroidism who have experienced a stressor, like an
infection, trauma, untreated DKA, or manipulation of the thyroid gland during surgery
Hallmark sign: High Fever of 105-106 F (40.5-41.1 C).
Thyroid storm manifestations

S – systolic hypertension
T – Tachycardia
O – over exhausted
R – restlessness, agitation, tremors, confusions, psychosis, delirium and seizures
M – More G.I. signs : Nausea vomiting, abdominal pain, DIARRHEA
Nursing interventions for thyroid storm

 Mortality rate is HIGH, Rapid treatment is essential to preserve life!!!!
 Cooling patien, NO ASA(aspirin), replace fluid & electrolytes, reduce TH synthesis.
 monitor HR, BP, RR (respiratory failure)
 keep environment cool, quiet (cooling blankets and sedatives as prescribed)
 NO foods with iodine (Kelp/seaweed, diary, eggs)
 Administer medications: goals decrease thyroid hormone levels, fever, effects of
increased hormones on body and prevent further secretion and conversion of thyroid
hormones
Medications for thyroid storm
1. Antithyroid medications: blocks SYNTHESIS (like
Tapazole/Methimazole)..fewer side effects
2. PTU (propythiauracil) – to decrease thyroid hormone
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3. Iodide solution: blocks SECRETION of TH (like Lugol's solution=taste changes

metal taste)
4. Tylenol (no salicylates) – FOR FEVER
5. Beta blockers like Inderal (not for patients with asthma or history of
bronchospasm) – Medications for thyroid storm that decrease effects of thyroid
hormone on the body by blocking peripheral conversion of T3 and T4
6. Glucocorticoids like Dexamethasone — Medications for thyroid storm that
prevent further secretion and conversion of thyroid hormones by suppressing
immune system
2. HYPOTHYROIDISM
Hypothyroidism involves decreased work of the thyroid gland which can affect body
metabolism.
 HIGH TSH , LOW T3 & T4
 More common in WOMEN above 65 years old
A. Primary Hypothyroidism
 Due to disease in the thyroid
The most common cause is autoimmune (Hashinmoto's thyroiditis)
Goiter does develop
B. Secondary Hypothyroidism
 Occurs when the hypothalamus produces insufficient thyrotropin-releasing hormone
(TRH). Goiter does not develop
Hypothyroid Risks factors

1. Thyroid surgery, neck radiation, & anti-thyroid meds
2. Iodine deficiency
3. Hashimotos thyroiditis- autoimmune disorder- MOST COMMON CAUSE
HYPOTHYROIDISM.
4. Pituitary tumor: stops anterior pituitary gland from secreting TSH
5. Treatment of hyperthyroidism: radioactive iodine or anti-thyroid medication
HALLMARK: DECREASE BODY METABOLISM — WEIGHT GAIN
SIGNS AND SYMPTOMS:
H – hypothermia or Cold intolerance
Y – yellowish or pale skin with DULL FACE
P – Poor wound healing and paresthesia’s
O – Ocular /Periorbital edema with non pitting edema of hands and legs
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T – Thick, brittle nails, Thick, dry scaly skin, Thick tongue

H – HYPOTENSION , Bradycardia and decrease C.O,
Y – you may have lethargy,, apathy, slow speech, decreased LOC and DEPRESSION
R – RECEDING or decreasing hair, with loss of eyebrow hair
O – Ototoxic (hearing loss)
I – ileus, CONSTIPATION
D – Decreased activity tolerance, muscles weakness, fatigue, decrease DTR
I – Impotence and Decreased libido in men
S – Slurring of speech (hoarseness) and Slowing of intellectual functions with inattentiveness
M – Menorrhagia and amenorrhea
Hypothyroidism Diagnostic Tests

 Ultrasound of the thyroid
 24 hour radioactive iodine uptake test
 Thyroid scan
Hypothyroidism Nursing Diagnosis
1. Ineffective Breathing Pattern (1st priority)
2. Decreased Cardiac Output (2nd priority)
3. Disturbed Thought Processes (3rd priority)
4. Activity Intolerance
5. Imbalanced Nutrition; More than body requirements
Hypothyroid Treatment
Drug of choice: levothyroxine (Levothyroid, Synthroid)
S – Synthetic thyroid hormone
Y – you take it in the MORING empty stomach, at least 30 minutes before breakfast.
N – NEVER abruptly stop med.
T – try to take the medicine at the same time each day
H – heart palpitations, chest pain or HR > 100 beats/min experienced should be reported
immediately.
R – Risk for bleeding when used with WARFARIN
O – observe for CARDIAC DYSRHYTHMIA (adverse effect)
I – insomnia, increase appetite, weight loss , sweating, headache and hyperactivity are side
effects
D – DAILY use and LIFELONG
WOF: Myxedema coma (coma with hypothermia)

Myxedema Coma – a potentially life-threatening complication of hypothyroidism.
Causes of myexedema coma:

*risk factor: elderly women with long history of hypothyroidism
*sedatives
*anti-thyroid medication toxicity
*not taking hormone replacements
*thyroidectomy
Signs and symptoms of myexedema coma

*typical s&s of hypothyroidism but SEVERE
*hypothermia (temperature 24° to 32.2° C),
*myedema: swelling of tissues that has a waxy appearance or orange peel texture on
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eyes and face

*bradycardia
*very drowsy/coma
*hypoglycemia: due to decreased metabolic rate, hence decreased gluconeogenesis
*hyponatremia: increased antidiuretic hormone which causes body to conserve water
and decrease glomerular filtration rate (decreased blood to kidneys)
*respiratory failure (hypercapnia) (most likely need mechanical vent)
Nursing interventions for myexedema coma
*ICU-monitor heart rate, blood pressure, EKG, temperature, and respiratory status
*administered as ordered: IV fluids for hyponatremia and correct cardio collapse
IVF of choice: normal or hypertonic saline
*IV Synthroid: can cause adrenal insufficiency by increased metabolism of
glucocorticoids...corticosterioids as ordered
*NO SEDATIVES – increase risk of coma
*warming blankets
*IV glucose if needed
Hypothyroidism Management
 Avoid exposure to cold and drafts provide extra clothing and use of warm blankets)
 Avoid and discourage the use of external heat source (e.g., heating pads, electric or
warming blankets)
 Space activities to promote rest and exercise as tolerated.
 Encourage increased fluid intake within limits of fluid restriction. Provide foods high in
fiber
 Monitor respiratory rate, depth, pattern, pulse oximetry, and arterial blood gases.
 Avoid the use of hypnotic, sedative, and analgesic agents risk for myxedema
Parathyroid Glands — very vascular, 4 small glands embedded into the POSTERIOR thyroid
Hormone: PTH – regulates calcium
 stimulates osteoCLASTS (breaks down bones) causing bone resorption which causes
hypercalcemia.
 stimulates bone TO RELEASE calcium
 renal reabsorption of calcium,
 Renal conversion of Vit D to active form
Hyperparathyroidism
 over secretion of PTH
 more common in WOMEN
 30-70 peaks at 40-50
Three classifications
1. Primary Hyperparathyroidism
 Over secretion of PTH
 benign tumor (adenoma)
 head and neck radiation
 Long term lithium treatment
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2. Secondary Hyperparathyroidism
 vit D deficiency
 malabsorption
 CKD (chronic kidney disease)
 Hyperphosphatemia
 renal patients
3. Tertiary Hyperparathyroidism
 caused by hyperplasia of the gland
 secretion of PTH even with normal levels of Ca,
 Kidney transplant under long term dialysis
Diagnostics
-PTH levels are elevated
-calcium levels are over 10 (hallmark sign)
-phosphorous is less than 3
-DEXA (duel energy x-ray) scans for bone density
-MRI, CT for tumor screening
-treatment depends on severity
S/S of hyperparathyroidism
- BONE FRACTURES: bone fractures/osteoporosis because more calcium in blood than in
bone.
- Calculi: renal stone formation (nephrolithiasis): kidneys absorbs calcium
- CONSTIPATION: GI system smooth muscles slow down (less calcium in organ and more in
blood)
- GI problems: calcium increases gastric acid level which causes N&V, epigastric pain
Frequent urination: increased calcium cause kidney to work harder (DEHYDRATION which
causes concentrated urine which causes renal stone formation).
EKG changes: SHORT QT intervals
MUSCLE WEAKNESS: particularly in proximal muscles of the lower extremities
Serious effects: renal failure, pancreatitis, cardiac arrhythmia, and fractures
Nursing Interventions for hyperparathyroidism

- monitor VS, EKG, urine (strain - watch for kidney stones, flank pain), calcium and phosphate
levels, I/O, encourage fluids (try to keep diluted)
- diet: low calcium and high phosphate (NOT for renal impaired patients: their phos levels are
already high-do NOT encourage high phos diet for renal impaired patients)
Treatments for hyperparathyroidism

- for PRIMARY cause
- parathyroidectomy (for primary cause): monitor RESPIRATORY STATUS!!: placed in
SEMIFOWLER position (relieves strain on cervical site, prevents excessive swelling, and
promotes drainage); TRACH KIT AT BEDSIDE, suction, oxygen.
- watch calcium levels (may go into hyPOcalcemia after surgery: tingling, numbness, excessive
twitching, positive trousseau's and Chvostek's sign)
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risk of tetany from sudden drop in calcium (tingling, spasms, laryngospasms, keep calcium
gluconate (increase threshold for cardiac arrythmia) available, assess chvostek's and
trousseau's sign.
- watch for LARYNGEAL NERVE DAMAGE! (problem speaking and swallowing)
medications for hyperparathyroidism
- goal of these meds?
- goal: decrease parathyroid hormone and decrease calcium (KEEP PT HYDRATED)
- Calcimimetics: sensipar (cinacalcet)prescribed for pt with SECONDARY cause (CKD):

- it DECREASES PTH, CALCEMIA, and PHOSPHATE levels as well (because renal patients
have HIGH phos levels):
- TAKE WITH FOOD.
- Mimics role of Ca and deceives parathyroid gland, thinking there's "enough Ca".
- Calcitonin: injection or nasally

- naturally produced by thyroid gland
- lowers calcium levels; suppresses osteoclast activity (stops bone from breaking down)
- causes kidney excretes calcium
- loop diuretics (LASIX): decrease Ca levels inhibiting Ca resorption in renal tubules (watch for
POTASSIUM LEVELS)
- Biphosphates (Pamidronate or Alendronate (Fosamax)): helps protect bones from losing Ca;
slowing osteoclasts and increasing osteoblasts
- Fosamax: take with EMPTY STOMACH; FULL GLASS of H2O, SIT UP RIGHT for 30
minutes after (because fosamax can cause severe ulcers in esophagus and stomach)
- wait 30 minutes before taking vitamins/antacids.
2. Hypoparathyroidism -uncommon condition, usually lack of PTH

-results in hypocalcemia
-most commonly iatrogenic (caused by physician treatment or surgery): inadvertent removal of
thyroid gland, damage to vascular supply
-genetic: pseudohypoparathryoidism (PTH ok)
-idiopathic: rare, childhood, anti-parathyroid antibodies
-others: chronic low magnesium, heavy metal poisoning, tumors
Signs and Symptoms
Tetany: sudden decreases in calcium concentration
-Tingling of the lips, fingertips, and occasionally feet
-Increased muscle tension leading to paresthesia’s and stiffness
-Laryngospasms
-Positive chvostek sign
-Positive trousseau sign
-Pts. are usually anxious and apprehensive
Diagnostic Studies
-Serum calcium and PTH levels decrease
-Serum phosphate levels increase
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Collaborative Care
-Treat tetany when present
-Prevent long-term complications by maintaining normal calcium levels
-Emergency treatment of tetany requires administration of IV calcium. Calcium can cause
hypotension and CA; thus a slow IV push is required
-Long term management, oral calcium supplements may be prescribed
-Specific hormone replacement of PTH is not used to treat hypoparathyroidism bc of the
expense and the need for parenteral admin
Nursing care
tx acute complications
-tetany
-administer IV Ca carefully (always diluted and slow rate)
-high Ca can cause *cardiac dysrhythmias and phlebitis
-extravasation can cause necrosis
-monitor cardiac function, muscle cramping, rebreathing (increase CO2, decrease pH, low pH
ionize Ca)
-teach long term drug therapy: Ca supplements, vitamin D (rocalcitrol), cannot absorb Ca
without vitamin D
rebreathing
-reduces CO2 excretion from lungs
-increase carbonic acid in the blood
-lowers pH to support ionization of Ca
-ionized Ca is active form
monitor
-cardiac function, muscle cramping, dysphagia, laryngospasms
teach long term drug therapy

-Ca supplements
-Vit D (rocalcitrol)
diet therapy
-green leafy veggies
-avoid spinach and rhubarb d/t oxalic acid inhibiting Ca absorption
-comply w/ Ca lab checks
THYMUS GLAND
Shape: pyramid-shaped lymphoid organ
Called thymus because its shape resembles that of a thyme leaf.
Color: Pinkish-gray
Location: lies in the mediastinum behind the sternum and between the lungs
Hormones: Thymosin, thymolin, thymopoietin
Thymosin for production of T lymphocytes (Develops immune system)
 aids in the production of lymphocytes (WBC) known as Tcells
 regulates the body's immune system
 site of maturation for t cells.
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Myasthenia Gravis
 a progressive autoimmune disease that produces severe muscular weakness.
 It is characterized by periods of exacerbation and remission.
 most treatable neurologic disorders.
 Muscle weakness during activity and improves with rest
 No it is NOT contagious.
 It is NOT a lethal disease like ALS is.
 You should live as long as you would have without it.
 Although it is rare, it is possible to die from complications caused by choking, or
respiratory failure
Most common affected muscles by MG:
 Eye muscle controlling eye movement
 facial expression
 chewing
 talking
 swallowing.
Onset: Both sexes
Females 15 to 35 years of age
Males 40 to 70 years of age
Cause of MG: caused by antibodies that interfere with the transmission of acetylcholine at the
neuromuscular junction.
Risk Factors - rheumatoid arthritis, scleroderma, and systemic lupus erythematosus
Factors that trigger exacerbations

- Infection
- Stress, emotional stress/upset, and fatigue
- Pregnancy
- Increases in body temperature (fever, sunbathing, hot tubs)
-erratic sleep habits
-overeating
- crowds
PRIORITY NURSING DIAGNOSIS: Ineffective breathing patterns related to weakness of chest

muscle and fatigue
SIGNS AND SYMPTOMS:

Hallmark of MG: muscle weakness that increases with fatigue.
 Is muscle weakness that worsens after periods of activity and improves after
periods of rest.
 CHARACTERISTIC: FATIGUE & DESCENDING MUSCLE WEAKNESS
 Progressive weakness that is worse at the days end. The client with myasthenia
develops progressive weakness that worsens during the day.
 FIRST/EARLY sign of MG: double vision (diplopia), and droopy eyelids (ptosis) are
usually among the first
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clinical manifestations of MG
W - weakness of neck, face, arms, legs
E - eye drooping "ptosis:
A - appearance mask like
K - Keep choking/gagging/difficult to chew and ⁸swallow
N - No energy/fatigue
E - Extraoccular movement - strabismus and diplopia
S - slurred speech/hoarseness of voice
S - shortness of breath - Myasthenia crisis (respiratory dysfunction)
Most significant initial nursing observations: Ability to chew, SWALLOW and speak
distinctly
 Muscle weakness can lead to respiratory failure that will require emergency intervention
and inability to swallow may lead to aspiration.
 To prevent aspiration of food, the nursing action that would be most effective would be
to: Coordinate her meal schedule with the peak effect of her medication.
 COLLABORATE with: Speech therapists – address swallowing problems, and clients
with myasthenia gravis are dysphagic and at risk for aspiration.
Diagnostic Procedures
 Tensilon testing – BEST CONFIRMATORY TEST
 Electromyography –shows neuromuscular transmission in MG, more sensitive but does
not rule out other causes.
 Serum assay for circulating Ach receptor antibodies — non conclusive
Tensilon testing
 Baseline assessment of the cranial muscle strength is done.
 Edrophonium chloride (Tensilon) is administered.
 Medication inhibits the breakdown of acetylcholine
 TENSILON increases muscle strength
 Tensilon or Edrophonium test will confirm myasthenia gravis. About 30 seconds after
being injected, muscle weakness is profoundly relieved ONLY FOR 5 minutes.
 + TENSILON TEST – results in marked improvement in muscle strength that lasts
approximately 5 min.
 Can be used to differentiate cholinergic crisis and myasthenic crisis.
 DRUG ALERT: TENSILON can cause dysrhythmias and cardiac arrest
 Have an ATROPINE always available (ANTIDOTE OF TENSILON)
 Signs of toxicity: (bradycardia, sweating, and abdominal cramps).
Upon injection of Tensilon:

 Myasthenic crisis – symptoms temporarily relieved
 Cholinergic crisis – symptoms worsens or remain unchanged.
Medications
1. Anticholinesterase agents – FIRST LINE TREATMENT
- Pyridostigmine (Mestinon) and neostigmine (Prostigmin)
- Neostigmine (Prostigmin). This drug acts by: Blocking the action of cholinesterase
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2. Immunosuppressants such as azathioprine (Imuran) and prednisone (Deltasone)

- Decreases the production of autoantibodies that attack the acetylcholine
receptors
- Long term use causes INFECTION, CATARACT, OSTEOPOROSIS
3. IV immunoglobulins (IVIg) - acute management

AVOID : PROCAINAMIDES –IT INCREASES WEAKNESS
Anticholinesterase agents- Nursing Considerations
M – medication is given at the specified time - usually 4 times a day.

E – Eat within 45 min of taking the medication to strengthen chewing and reduce the risk for
aspiration.
S – Same time each day to maintain therapeutic levels
T– Take with food to address gastrointestinal side effects. (milk and/or crackers)
I – If periods of weakness are observed, discuss change in administration times
with the provider.
N – NOT to be given to pt. with intestinal obstruction or urinary tract, peritonitis, &
hypersensitivity
O – observe for signs of toxicity of neostigmine, ATROPINE should always at the bedside
N – Neostigmine or Pyrostigmine best time to administer is 30 minutes before meals
(Peak response occurs 1 hour after administration and lasts up to 8 hours.
MYASTHENIC VERSUS CHOLINERGIC CRISIS

1. Myasthenic crisis — caused by undermedication ,overexertion and overeating
Management: administration of cholinergic medications, such as neostigmine (Prostigmin)
and pyridostigmine (Mestinon).
WOF: Respiratory distress
Note: Insert NG tube, Inserting the NG tube will help reduce risk for aspiration. The patient
experiencing a myasthenic crisis is at a large risk for respiratory failure due to dysphagia
and extreme muscle weakness.
2. Cholinergic crisis — caused by excess medication
Management: withholding of medications for 1 to 3 days and administration of ATROPINE
SULFATE (antimuscarinic and antichollinergic drug)
Priority / TOP nursing diagnosis: Ineffective airway clearance
 During a cholinergic crisis, secretions are increased and the gag reflex is decreased
Prevention of myasthenic and cholinergic crises. : Taking medications on time to maintain

therapeutic blood levels
Plasmapheresis
 Remove antibody-antigen complexes from circulation
 Plasmapheresis can be used to remove the antibodies from the circulation.
 Plasmapheresis is used in SLE, MG, GBS to remove antibodies, antibody-antigen
complexes
 Monitor for ELCTROLYTE panel after procedure, assess for numbness and tingling
sensation (hypocalcemia)
 WOF: lightheadedness and dizzimess (sign of hypovolemia)
Nursing Care for patients with Myasthenia Gravis
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M – maintain a patent airway (muscle weakness of diaphragm, respiratory muscles)

Y – Yes! Patient must WEAR medical ID bracelet at all times
A – assess swallowing to prevent aspiration.
S – suction apparatus, oxygen, endotracheal intubation, and a bag valve mask available at the
client's bedside.
T – take meds at specified times
H – High calorie meals and SOFT DIET, keep water in bedside early morning
E – Energy conservation measures. Allow for periods of rest.
N – need lubricant eye drop during day and EYE PATCH at night (prevent corneal damage)
I – Intubate patient when in respiratory distress.
A – assume fowlers position or sit upright when eating
SURGERY: THYMECTOMY
 A thymectomy removes the thymus gland.
 performed EARLY COURSE of the disease.
 help reduce symptoms but the effects may not be seen for many months after surgery.
PURPOSE: Eliminate the source of AChR antibodies
Post-thymectomy WOF: symptoms of pneumothorax or hemothorax, which include sudden
shortness of breath, chest pain, and diminished breath sounds.
CUSHINGS DISEASE (Harvey Cushing)
 Cushing's: hyper-secretion of CORTISOL (think Cushing and Cortisol both start with
C's)
PITUITARY GLAND – focal structure affected
CAUSE: Pituitary Adenoma
Risk factor: patient taking glucocorticoids for several weeks.
Cushing's syndrome & Cushing's disease
1. Cushing's Syndrome: caused by an OUTSIDE SOURCE or medical treatment
such as glucocorticoid therapy (prednisone) (70% of cases)
2. Cushing's Disease: caused from an INSIDE SOURCE due to the pituitary gland
producing too much ACTH (Adrenocorticotropic hormone) which causes the
adrenal cortex to release too much cortisol.
 *pituitary glands or adrenal cortex, or genetic predisposition
MUST KNOWS:
 The disease occurs in WOMEN between 20 to 40 year of age.
 The use of Corticosteroids for multiple immune conditions is a cause of the disease
process.
 Condition is aggravated by excessive production of ACTH.
 The surgical treatment of choice is Transsphenoidal hypophysectomy
REMEMBER COSRTISOL is stress hormone

Hallmark signs of Cushing syndrome —buffalo hump, a rounded face, and pink or purple
stretch marks or striae
SIGNS AND SYMPTOMS
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S – skin fragile easy bruising and poor wound healing due to thin and atrophic skin, acne
T – truncal obesity (protuberant abdomen) with thin extremities
R – rounded face (moon face), kyphosis and back pain
E – ecchymosis, Elevated blood pressure
S – striae on the extremities and abdomen (Purplish)
S – sugar extremely high (hyperglycemia)
E – excessive body hair(Hirsutism) and Electrolytes imbalance: hypokalemia
D – dorsocervical fat pad (Buffalo hump) and depression (labile mood), decreased libido,
changes in menstrual cycle
RISK FOR : OSTEOPOROSIS – Bone matrix demineralization
*NOT sign of Cushing’s Decreased or absent pubic hairs and Hyperpigmentation of the
skin (sign of Addisons)
CUSHINGOIDS FEATURES (7 H)
H – hypercortisolism
H – hypertension
H – hyperglycemia
H – hypercholesterolemia
H – hirsutism
H – hypernatremia & Hypokalemia
H – high risk for infection
 Cushing's syndrome causes sodium retention, which increases urinary potassium loss.
 Therefore, the nurse should advise the client to increase intake of potassium-rich foods,
such as fresh fruit.
 The client should restrict consumption of dairy products, processed meats, cereals, and
grains because they contain significant amounts of sodium.
Diagnosis: CT scan and MRI to detect non hemorrhagic injury in the brain.
Cortisol and ACTH (adrenocorticotrophic hormone) level.
Blood Cortisol Testing – done early in the morning
Salivary cortisol test – late night (10-11pm)
Normal: 150 or less + cushings: greater than 250
Confirmatory test: 24 hour urinary free cortisol
Main test: overnight dexamethasone suppression test
for the overnight dexamethasone suppression test 1mg of dexamethasone is given and 11 pm
and serum cortisol levels are checked at 8 am the next day (<1.8) is negative
COLLABORATIVE APPROACH: Dietician – for nutritional planning

Diet for Cushing should include: fluid restriction (body holding on to fluid), increase protein
(help with wound healing), increase potassium (Cushing manifestation is hypokalemia),
decrease sodium (Cushing manifestation is HYPERnatremia), & decrease fat
Treatment of choice: Transsphenoidal surgery for pituitary tumors and adrenalectomy for
adrenal tumors
*Spirinolactone for hypertension
Surgery – pituitary is depressed 6 to 36 nonths after surgery
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INTERVENTIONS
 Monitoring daily weight
 Monitoring intake & output
 Maintaining a low sodium diet
 Maintaining high potassium diet
 Monitoring extremities for edema
Discharge Instructions:
 Carry or wear a medical identification bracelet
 Unnecessary exposure to high temps & emotional disturbances should avoided
 Signs & symptoms of infection must be reported
 High in protein, adequate potassium, low sodium & calories in the diet
 Instruct to report any signs such as hot, dry, flushed face
 Note any potential hazards for falls at home (loss of bone matrix)
 Get readings of BP twice a week and share w/HCP
 Suspect pulmonary edema for Crackles & is a PRIORITY. Inverted T waves would be
also a concern.
ADDISONS DISEASE (Thomas Addison )

Addisons – Hyposecretion of Aldosterone & Cortisol (Aldosterone & Addison's both start with
A's so Addison's effects both cortisol & aldosterone)
Adrenal glands – Affected focal structure
CAUSES:
Primary cause - hypofunction of the adrenal cortex
Secondary cause - lack of pituitary ACTH secretion.
OTHERS
 Autoimmune due to adrenal cortex
 Cancer
 Tuberculosis/infections (most common risk factor)
 Hemorrhaging of the adrenal cortex due to a trauma
Common in both genders in adults younger than 60 years old. (30 to 50)
In Addison's disease, what hormones are reduced:

All three classes of adrenal corticosteroids:
S - salt Mineralocorticoids (aldosterone)– regulates BP, sodium potassium transport
S - sugar Cortisol/Glucocorticoids (sugar)
S - sex androgens
PRIORITY NURSING DIAGNOSIS: RISK FOR INFECTION

ROOM: PRIVATE ROOM
Hallmarks:
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Hypotension/hypovolemia
Hyperpigmentation is one of the FIRST noticeable hallmark symptoms
weight loss, emaciation and fatigue
 Bronzed or smoky hyperpigmentation of face, neck, hands (especially creases) buccal

membranes, nipples, genitalia, and scar.
Signs and symptoms

*Remember the phrase: "Low STEROID Hormones"
S - sodium (hyponatremia) & Sugar low (hypoglycemia), Salt cravings

T - tired (fatigue)and muscle weakness
E - electrolyte imbalance: Hyperkalemia, hypercalcemia
R - reproductive changes: irregular menstrual cycle and Erectile dysfunction in men
O - obvious alopecia and decreased pubic hair
I - increased pigmentation of the skin (hyperpigmentation of the skin)
D – diarrhea, NV, cramping abdominal pain, and Depression
Diagnostic Studies
Synacthen stimulation test to confirm the diagnosis, uses tetracosactide chemical
 test of adrenal insufficiency, serum ACTH stimulation test
1. History and physical examination

2. Serum cortisol - low levels
3. Urine cortisol and aldosterone - Cortisol below normal range of 80 to 120 mcg/24 hr and
low Aldosterone would be a positive result for Addison's disease.
4. Serum electrolytes - hyperkalemia, hypochloremia, hyponatremia, hypoglycemia,
anemia, and increased BUN levels
5. MRI & CT Scan
MRI - used to identify causes other than autoimmune, including tumors, fungal
infections, tuberculosis, or adrenal calcification.
CT SCAN of BRAIN and ABDOMEN
Closely monitor:
Watch glucose and K+ level (less cortisol=lower glucose levels, b/c aldosterone is effected it
causes hyperkalemia)
Addison's DIET: High protein, carbs, and adequate sodium or low potassium, high sodium,
high, carbs-need enough calories (turkey and cheese sandwich)
Treatment
1. Daily glucocorticoid (to replace cortisol) like hydrocortisone, prednisone, replacement
(two thirds on awakening in morning, one third in late afternoon)*
2. Daily mineralocorticoid (fludrocortisone [Florinef]) in the morning* consume salt
3. Salt additives for excess heat or humidity
4. Increased doses of cortisol for stress situations (e.g., surgery, hospitalization)
Medications that can cause a need to increase glucocorticoid dosage
 Phenytoin
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 Barbiturates
 Rifampin
 antacids
Effects and Side Effects of Corticosteroids: CUSHING SIGNS & SYMPTOMS
P peptic ulcer disease.
R risk for infection (priority nursing diagnosis)
E elevated BP (HTN)
D delayed wound healing and easy bruising
N Na and water retention (weight gain)
I increases sugar (DM)
S triaes and skin purpura
O steoporosis and pathologic fractures
N ausea and vomiting
E yes and nose: glaucoma, cataracts and nosebleed.
WOF: Addisonian Crisis - life-threatening emergency requiring aggressive management.

Cause: NOT taking their prescribed hormone therapy replacement/abruptly stopping
medications
High risk: post-opt adrenalectomy.
Addisonian Crisis the 4'H (hypoglycemia, hypotension, hyponatremia, and hyperkalemia).
Management: administer cortisol immediately best example: IV Solu-Cortef ( Prednisone is
not the best in crisis)
IVF of choice: Large volumes of Normal Saline solution or D5W (to reverse hypotension and
electrolyte imbalances until BP returns to normal.)
Highest priority Nursing diagnosis: Decreased cardiac output
Priority Assessment: Vital signs every 30mins in the first 24 hours of crisis
Addison’s disease – Teaching Plan

1. Names, dosages, and actions of drugs
2. Symptoms of overdosage and underdosage
3. Conditions requiring increased medication (e.g., trauma, infection, surgery, emotional
crisis)
4. Course of action to take relative to changes in medication
• Increase in dose of corticosteroid
• Administration of large dose of corticosteroid intramuscularly, including demonstration
and return demonstration
• Consultation with health care provider
5. Prevention of infection and need for prompt and vigorous treatment of existing
infections
6. Need for lifelong replacement therapy
7. Need for lifelong medical supervision
8. Need for MEDIC ALERT bracelet
9. Prevention of FALLS
10. Special instruction for patients who are diabetics and management of blood glucose
when taking corticosteroids
Addison’s disease – Teaching patient and caregiver to manage corticosteroid therapy
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1. Plan a diet high in protein, calcium (at least 1500 mg/day) and potassium but low in
fat and concentrated simple carbohydrates such as sugar, honey, syrups, and candy.
2. Identify measures to ensure adequate rest and sleep, such as daily naps and
avoidance of caffeine late in the day.
3. Develop and maintain an exercise program to help maintain bone integrity.
4. Recognize edema and ways to restrict sodium intake to <2000 mg/day if edema
occurs.
5. Monitor glucose levels and recognize symptoms of hyperglycemia (e.g., polydipsia,
polyuria, blurred vision). Report hyperglycemic symptoms or capillary glucose levels
>120 mg/dL (10 mmol/L).
6. Notify health care provider if experiencing heartburn after meals or epigastric pain that is
not relieved by antacids.
7. See an eye specialist yearly to assess for cataracts.
8. Use safety measures such as getting up slowly from bed or a chair and use good
lighting to avoid accidental injury.
9. Maintain good hygiene practices and avoid contact with persons with colds or other
contagious illnesses to prevent infection.
10. Inform all health care providers about long-term corticosteroid use.
11. Recognize need for increased doses of corticosteroids in times of physical and
emotional stress.
12. Never abruptly stop the corticosteroids because this could lead to addisonian crisis and
possibly death.
13. Increase calcium intake, vitamin D supplementation, biphosphonates – alendronate, and
low impact exercise to reduce bone resorption
14. Dental work can be a cause of physical stress; therefore, the client's physician needs to
be informed about the dental work and an adjusted dosage of steroids may be
necessary.
15. Daily weights should be monitored to monitor changes in fluid balance
DI versus SIADH
1. Diabetes insipidus.
D.I. – Abnormal excretion of large volumes (>3L) of DILUTE urine related to UNDER
production of VASOPRESSIN (ADH).
Posterior Pituitary gland — affected part

Cause: DEFFICIENCY OF VASOPRESSIN
Most frequent cases of DI caused by: defect in the hypothalamus or pituitary
- trauma, irradiation, cranial surgery
3 types of Diabetes Insipidus

1. Neurogenic or Central — caused by damage to hypothalamus or Pituitary gland
 Concussions (head injury or trauma)
 Brain Tumor, CNS infection, brain surgery.
 DRUGS: Ethanol, opiate antagonist, phenytoin
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2. Nephrogenic — Decreased renal response to ADH

 Lithium therapy, amphtericin B, renal damage, hereditary (X -linked congenital)
renal disease
 Treatment: thiazide diuretic
3. Psychogenic — Associated with excessive water intake. Caused by structural lesion

in thirst center or psychiatric problem.
 beer or water potomania, Excessive water intake (>5L/day) Lesion in thirst
center. Psychiatric disorder(schizophrenia)
Triphastic Period of Central DI

 Acute phase- Abrupt onset of polyuria, falling urine specific gravity (lasts 4-5
days)
 Interphase- Urine output apparently normalizes due to antidiureses as stored
ADH is released (Lasts 5-6 days)
 Third Phase- ADH can no longer be released due to stores being exhausted or
damaged hypothalamus's inability to produce ADH, if not corrected, DI can
become permanent
Hallmark sign of D.I.: Polyuria Polydipsia, low urine specific gravity (less than 1.005 or
urinary osmolality of less than 200 mOsm/kg)
Signs and symptoms:

 Polyuria — urine output of more than 3 L per day (5 - 20 L/day)
 Polydipsia — intake of 4 - 30 L/day
 Dehydration (FVD)
 Hypovolemic Shock
Signs of dehydration
FIRST/EARLY SIGNS: EXCESSIVE THIRST and Dark colored urine
 D - decreased blood volume (hypotension)

 E - elevated temperature
 H - headache
 Y - you may be dizzy and lightheaded
 D - dry mucous membranes
 R - respiratory rate may increased
 A - abnormally sleepy or lethargy
 T - tachycardia
 E - eyeballs are sunken
 D - decreased skin turgor
Signs of hypovolemic shock

 HYPOtension
 TACHYcardia
 TACHYpnea
 decreased CO
 decreased cerebral perfusion
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DIAGNOSIS: Water deprivation test is the best test to diagnose central diabetes insipidus.
 NPO, and vital signs, urine osmolality and weights will be done hourly until the end of the
test.
Lab findings for Diabetes Insipidus

 Urine dilute---->
Specific gravity < 1.005
Low osmolality (50 - 200)
Decreased pH
Decreased urine sodium
Decreased urine potassium
Increased serum osmolality (>295 mosm/kg.)

Increased serum sodium and potassium (because of increased serum osmolality)
ELECTROLYTE IMBALANCE:
1. HYPERNATREMIA – confusion, neuromuscular excitability, hyperreflexia,
disorientation, lethargy seizures, and coma.
2. HYPOKALEMIA — muscle cramps, muscle weakness, prominent U wave,
depressed ST segment
Goal of treatment with DI: to maintain fluid and electrolyte balance

IVF of choice: IV hypotonic saline or dextrose 5% in water to replace urine output.
Drug of choice with DI: Vasopressin drug — desmopressin (DDAVP)
Diuretic of choice: thiazide diuretic (it makes the body retain salt)
First intervention for a pt. with DI: monitor vital signs and neuro status
Monitor in D.I.: sodium and potassium
Check sodium serum levels and urine specific gravity: q 2 - 4 hr
Must be in the bedside for a pt. with DI: Fluid
Check outputs: q 1hr
Nursing management and goals

 IV fluids needed to match output and correct electrolytes
 Prevent dehydration and shock
 Assess skin turgor q4 hours
 Weight daily
 Encourage fluids as tolerated
 Avoid caffeine products that promote further diuresis
 Monitor for dehydration (mental status, skin turgor, etc.)
 Administer IV fluid, hourly I's and O's
 Monitor Na levels and serum osmolality
 Monitor BP, HR, mental status, urine specific gravity
 Assess response to DDAVP therapy
Discharge priorities Patient instruction:
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 Importance of hydration
Postoperative and medication instructions
 Weigh every morning
 Wear an identification (medic alert) bracelet at all times
notify the health-care provider for chest tightness
 Follow-up evaluation
 Emotional support
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

SIADH — A syndrome characterized by EXCESSIVE release of ADH from the posterior
pituitary gland.
SIADH CAUSE: EXCESSIVE ADH release
MOST COMMON CAUSE: Malignancy, especially small cell lung cancer.
CNS Disorders: Trauma, Infection, Tumors, Strokes, SLE
Malignant tumors: Small cell lung cancer, Hodgkin's lymphoma, NHL, Pancreatic/Duodenal?
GU carcinomas
Cancer cells are capable of producing, storing, and releasing ADH independently
Pulmonary disorders: Viral/Bacterial pneumonia, Lung abscesses, Mycoses, Chronic lung
diseases
Drugs: Chlorpropamide, Carbamazepine, Opioids, Vincristine, TCA's,SSRI
MAIN PROBLEM IN SIADH: FLUID VOLUME EXCESS OR FLUID OVERLOAD

 Water retention – NO edema in SIADH
 Water intoxication (FVE) – CHECK neck or jugular vein distention
 Dilutional hyponatremia
Signs of fluid volume excess

weight gain without edema
crackles in the lungs
distended neck veins
taut skin
tachycardia
HTN
Hallmark sign of SIADH: HYPONATREMIA

Early sign of hyponatremia: HEADACHE
Major electrolyte imbalance in SIADH: Dilutional HYPONATREMIA
 Fatigue, lethargy, headache, mental confusion, altered level of consciousness, anxiety,
coma, anorexia.
WOF: Confusion and seizures (Cerebral edema), classic signs of water intoxication
SIADH SIGNS AND SYMPTOMS:

Early S/sx: G.I disturbances anorexia, nausea and vomiting.
Late S/sx: Personality changes, confusion, decreased DTR, seizures, coma/death
SIGNS AND SYMPTOMS OF SIADH

B: weight gain (bloated)
L: long time between voids
O: overabundance ADH
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A: anorexia
T: tachycardia
E: electrolyte imbalance(Hyponatremia)
D: disorientation
7 S's of SIADH
1. Stop's urination (low urine output)
 Urine concentrated - specific gravity >1.025 - High osmolality - Increased urine sodium
and potassium. Serum (blood) concentrated
2. Sticky & thick "urine" HIGH Sp. Gravity 1.030+
3. Soaked inside "low & liquidy" labs
-HYPO osmolality (low)**
-HYPOnatremia below 135 Na+ (sodium)
4. Sodium low! (headache, early sign)
5. Seizures (key words: headache, confusion)
6. Severe high BP
7. Stop all fluids + give salt + diuretics
Laboratory and Diagnostic Tests

Decreased plasma osmolality < 280 mmol/kg
Increased urinary osmolality
Increased urinary specific gravity > 1.025
Increased urinary sodium
Clinical euvolemia (increased fluid without edema)
Weight gain
PRIORITY goal of SIADH: Maintenance of fluid and electrolyte balance

Treatment: Fluid restriction to 800 –1000ml/day
IV of choice: Hypertonic Saline (3%-5%) ex. 3%NaCl
Diuretic of choice: Loop diuretic such as furosemide (Lasix) ONLY if sodium level is near
normal already
Meds: Diuretics (Lasix when Na levels are near normal), Demeclcycline, Tolivaptan (PO) and
Conivaptan (IV)-causes water excretion without Na loss
Demeclocycline and lithium (inhibit the action of ADH on the renal collecting duct).
Demeclocycline blocks the action of antidiuretic hormone (ADH) on the renal tubules and
increases urine output.
Surgery- Hypophysectomy
Interventions and rationales

 Determine fluid balance every 8 hours; evaluate hydration status every 4 hours
 Monitor tissue perfusion status
 Review serum sodium, serum and urine osmolality
 Monitor ECG for dysrhythmias – wide QRS and Vfib
 Check CNS status - fall and seizure precautions for low Na
 Monitor, evaluate, and/or assist with breathing
 HOB low (10 degrees) - reduces ADH secretion
 Prevent decubitus ulcers - turning and joint mobility
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Adrenal gland / Suprarenal gland
FUNCTIONS: produce hormones that help regulate your metabolism, immune system,
blood pressure, response to stress and other essential functions.
MAIN FUNCTIONS
1. Regulation of fluid volume
2. Carbohydrate metabolism & stress response
Shape: triangular at Top of kidneys

Two glands located superior to each kidney
Location – superior poles of the kidneys..
Adrenal cortex – secretion of STEROID hormones (mineralocorticoids, glucocorticoids, and
androgens.)
Adrenal medulla – secretion of CATECHOLAMINES (epinephrine and norepinephrine)
Adrenal medulla {Fight-or-flight response}

 Adrenaline (epinephrine)
 Boost the supply of oxygen and glucose to the brain and muscles (by increasing heart
rate and stroke volume, vasodilation, increasing catalysis of glycogen in liver, breakdown
of lipids in fat cells)
 Dilate the pupils
Suppress non-emergency bodily processes (e.g., digestion) 
 Suppress immune system
 Noradrenaline (norepinephrine)
 Boost the supply of oxygen and glucose to the brain and muscles (by increasing heart
rate and stroke volume, vasoconstriction and increased blood pressure, breakdown of
lipids in fat cells)
 Increase skeletal muscle readiness.
PHEOCHROMOCYTOMA (paraganglioma)
phaios "dark“ chroma "color“ kyto s "cell“ -oma "tumor“
 A tumor that is usually benign and originates from the chromaffin cells of the adrenal
medulla ·
 Onset: 30 to 60 years old
Affected: ADRENAL MEDULLA (CHROMAFFIN CELLS)

Problem: EXCESSIVE CATECHOLAMINES
Catecholamine’s – regulates BP and HR
RULE OF 10’s
10% malignant
10% bilateral
10% Children
10% Men
10% Familial
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10% stroke person

10% found incidentally
10 % extra adrenal
10% calcified
10% recur
SIGNS AND SYMPTOMS

HALLMARK: HYPERTENSION
Triad of symptoms – Headache, Sweating, and Heart palpitations
5H
Hypertension – fluctuating, intermittent or paroxysmal ( rapid onset and abrupt cessation) .
Hypermetabolism – diaphoresis, agitation, rapid pulse, palpitation, emotional outbursts.
Hyperglycemia
Headache
Hyperhidrosis
Acute attacks (profuse diaphoresis, dilated pupils, cold extremities, severe hypertension which
can precipitate stroke or sudden blindness).
S/Sx:
Facial flushing (from hypertension), fluttering in chest (palpitations)
*Increased blood pressure & heart rate
Glucose high
*Headaches (sudden and severe)
Tremors
*Frequent sweating (from hypertension)

Loss of weight
Increase anxiety and fear
Growing tumor can cause back or abdominal pressure or pain
Heat intolerance
Tired and weak (from the constant stimulation)
Signs and symptoms can happen in episodes or triggered after an event:

 Eating foods with Tyramine (plays a role in pressure blood): foods that are aged,
pickled, fermented like cheeses, red wine, smoke/dried meat, bananas,
sauerkraut, chocolate.
 Surgery, trauma injury, emotional stress, medications such as Monoamine
Oxidase Inhibitors: MAOIs
Diagnosis:
24 hour urine vanillylmandelic acid – most conclusive test
SPECIMEN: 24 hours urine (5ml)
Normal findings : < 7 mg/24 hr
AVOID: Coffee, tea (including decaffeinated varieties), bananas, chocolate, vanilla, and aspirin
Avoid emotional or physical stress
Avoid use of OTC or prescribed drugs (amphetamines, nose drops or sprays, decongestant
agents, bronchodilators)
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Blood test to measure metaneprhines. – MOST SENSITIVE AND CONFIRMATORY

+VMA – refer for MRI or CT scan to detect adrenal tumors
Clonidine suppression test reveals continued increased levels of plasma catecholamine.
Treatment:
Treatment Goal: To control blood pressure
Priority nursing action would be to monitor the: VITAL SIGNS (BP-HTN)
 Adrenalectomy: primary treatment,
 remove the adrenal gland with the tumor (may remove one or both depending on
where tumor is located)
 Pre-opt: prescribed alpha-adrenergic blockers
 priority in the first 24 hours after a bilateral adrenalectomy is:
■ Preventing adrenal crisis. – MONITOR VS
 Assess further signs also of Poor lung expansion — turn pt. , teach to cough and deep-
breathe every 1 to 2 hours, or more
 GIVE ANALGESIC for pain: Hydromorphone hydrochloride (Dilaudid)
 STEROID EXCESS is expected after adrenalectomy asses poor wound healing
NIRSING DIAGNOSIS:
1st priority : Decreased cardiac output related to increased vascular resistance/ vasoconstriction
2nd : Pain related to increased cerebral vascular pressure as manifested by headache
3rd: Activity Intolerance related to body weakness
4th: Knowledge deficit related to lack of information about the disease process and self-care
Treatment:
1. Alpha blockers/ alpha-adrenergic antagonist: Phentolamine (regitine)

 Phentolamine (regitine) – FIRST LINE TREATMENT
 phenoxybenzamine (Dibenzyline), doxazosin (Cardura), prazosin (Minipress)
and terazosin (Hytrin).
2. Beta blockers/ beta-adrenergic blocking agents
 make the heart beat more slowly and with less force
 Blocks the effects of the hormone norepinephrine.
 slow down the release of the enzyme renin from kidneys
 keep blood vessels dilated.
 Examples of beta blockers include Atenolol (Tenormin), Metoprolol (Lopressor,
Toprol XL) and Propranolol (Inderal LA).
 PROPANOLOL – First line treatment of tachycardia
3. IV FLUID OF CHOICE: ISOTONIC, NORMAL SALINE

4. ADRENALECTOMY – removal of adrenal gland
PREOPERATIVE
 Pre-op: take alpha-adrenergic prior to surgery 2 weeks before surgery
 IV Phentolamine before surgery
 Risk for injury related to excessive release of catecholamines preoperatively
 Desired outcome is to prevent attacks of acute paroxysmal HTN
 Position on OR TABLE in LATERAL DECUBITUS
 Promote rest and relief from stress
 Sedatives
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 Prohibiting beverages containing caffeine such as coffee, tea, cola

 monitor vitals
POST OPERATIVE:
 Risk for injury related to postop hypotension, hemorrhage and shock
 During immediate postop period, monitor for shock and hemorrhage
 Give IV fluids ( blood,plasma, dextran, glucose in water to maintain blood vol
 monitor BP. Give vasopressors to MAINTAIN BP
 Carefully measure urine output ( oliguria indicates shock)
 Assess client for manifestations of hemorrhage (dressing for bloody drainage)
 If cortical tissue is resected during sx, assess client for manifestations of adrenal
insufficiency. If both glands removed.
 Client must receive cortical replacement for life
Bilateral adrenalectomy (both glands removed ): will have to take glucocorticoids and
mineralocorticoid FOR LIFE
Unilateral adrenalectomy (only one gland removed): will have to take glucocorticoids for
approximately TWO (2) YEARS
Nursing Interventions for Pheochromocytoma

A – Assess and MONITOR BP & HR, HYPERTENSIVE CRISIS may occur
D – Diet: High calorie diet, AVOID STIMULANTS: Caffeine/decaf, alcohol, tea, smoking
R – Risk for MI and stroke: assess chest pain , ECG
E – Ensure calm and cool environment, NO OVER STIMULATION (seizure)
N – No exercise, it increases catecholamine production.
A – AVOID PALPATION of the abdomen, may increase CATECHOLAMINES
L – lie on bed with head elevation to 45°
Complications
 HIGH BLOOD PRESSURE
 HEART ATTACK
 HEART FAILURE
 STROKE
 KIDNEY FAILURE
 COGNITIVE DECLINE
 DEMENTIA
 VISUAL IMPAIRMENT
PANCREAS – releases insulin and glucagon

Shape: flat pear or elongated
Length – 6 inches
Color: light tan or pinkish
Location: LUQ/Left Hypochondriac to EPIGASTRIC region
Two main functions:

Exocrine function – helps in digestion
Endocrine function – regulates blood sugar.
HORMONES
Glucagon — produce by ALPHA CELLS of Islets of Langerhans
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Insulin — produce by BETA CELLS of islets of Langerhans (most important hormone)
DIABETES MELLITUS
Diabetes — CHRONIC, metabolic disease characterized by HYPERGLYCEMIA
Organ affected: PANCREAS
SERIOUS DAMAGE: to the heart, blood vessels, eyes, kidneys and nerves.
Diabetes ranks FOURTH among the leading causes of MORTALITY (4TH TOP KILLER) in the
Philippines
TYPE 1 – JUVENILE ONSET
TYPE 2 – MATURITY ONSET
Key Players:
1. Glucose:
 “Sugar” (body needs it to survive) fuels the cells of your body
so they can work properly, BUT IT CAN NOT ENTER THE
CELL WITHOUT THE HELP OF INSULIN.
 It is stored mainly in the LIVER in the form of GLYCOGEN
2. Insulin:
 “deals with HIGH blood sugar levels”
 A hormone that helps regulate the amount of glucose in the
blood (too much glucose is very toxic to the body).
 It allows your body to use glucose by allowing it to enter the
cells (without insulin glucose would just float around in your
body)
 Secreted by the BETA cells of the pancreas from the ISLETS
OF LANGERHANS.
3. Glucagon:
 “deals with low blood sugar levels”
 A peptide hormone that causes the liver to turn glycogen into
glucose…does the opposite as insulin.
 Also secreted by the pancreas
Liver: Sensitive to insulin levels and stores and turns glycogen into glucose when the
pancreas secretes glucagon.
Example: (if the body has increased blood glucose/increased insulin in the blood the
liver with absorb and store the extra glucose for later….if there is low blood sugar/low
insulin levels the liver will release glycogen which turns into glucose to help increase the
blood sugar level)
Glucagon and Insulin Feedback Loop
Increased blood sugar -> pancreas releases insulin -> causes glucose to enter into the
cells to be used or be saved as glycogen for later (stored mainly in the liver)
Decrease blood sugar -> pancreas release glucagon -> causes the liver to release
glycogen which turns into glucose to increase the low blood sugar level
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What happens in diabetes mellitus?

 The body is unable to use glucose due to either the absence of insulin or the
body’s resistance to use insulin. Therefore, the patient
becomes HYPERGLYCEMIA (the glucose just hangs out in the blood stream
which affects major organs of the body)
 The body starts to metabolize FATS for energy (since it can’t get to the glucose…
remember glucose can NOT enter the cell without the help of INSULIN)….which
happens in Type 1 diabetics OR there is a moderate amount of insulin to deal with
fats and proteins BUT carbs cannot be used (Type 2).
Causes of Diabetes Mellitus
Divided into types:
1. Type 1: INSULIN DEPENDENT
 the beta cells located in the islet of Langerhans don’t work (been
destroyed) therefore the body doesn’t release anymore insulin.
 NO insulin production
 For treatment, the patient MUST USE INSULIN.
Risk factors: Genetic, auto-immune (virus) NOT RELATED TO LIFESTYLE (like type 2)
PATIENTS are THIN AND YOUNG, KETONES will be PRESENT IN URINE(KETONURIA)
2. Type 2: NON INSULIN DEPENDENT (95%)
 cells quit responding to insulin (won’t let insulin do its job by taking the
glucose into the cell).
 Therefore, the patient has INSULIN RESISTANCE.
 This leaves all the glucose floating around in the blood and the pancreas
senses there’s a lot of glucose present in the blood so it releases even
more insulin.
 Due to this the patient starts to experience hyperinsulinemia which caused
metabolic syndrome
Risk Factors: Lifestyle- being OBESE, sedentary, poor diet (sugary drinks), stress AND
genetic
Treatment: diet and exercise (first line treatment)…when that doesn’t work oral
medications are started Note:
 The type 2 diabetic may NEED INSULIN DURING STRESS, SURGERY, OR
INFECTION
 Patients are ADULT OVERWEIGHT or OBESE, it happens overtime, RARE OR
UNUSUAL to have ketones in urine
 Insulin resistance is a hallmark of Type 2 diabetes
3 of Hyperglycemia P’s & SUGAR

Hyperglycemia: Three P’s
Polyuria: (frequent EXCESSIVE urination)
 Why? elevated levels of glucose in the body causes the body to remove the water
from inside the cell HOWEVER, normally your kidneys could handle all of the
glucose by reabsorption but there is too much so it leaks into the urine
GLYCOSURIA
Polydipsia: very thirsty (EXCESSIVE THIRST)
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 Why? the blood is trying to prevent the body from becoming dehydrated from the
excessive urination so it signals to the patient to drink more water…but it doesn’t
work because the kidneys will remove the excess water
Polyphagia: very hunger (EXCESSIVE HUNGER)

 Why? the body is burning FAT for energy since it doesn’t have any glucose to use
so the body signals to the person to keep eating so there will be food to use for
energy. The patient will have WEIGHT LOSS!
*The 3 P’s present mainly in Type 1 Diabetics
Other S/Sx: “Sugar”
S – slowed wound healing

U – unwell vision (blurry)
G – glycosuria (kidneys can’t reabsorb all the extra glucose)
A – acetone smell of breath (from burning ketones) *type 1
R – rashes on skin DRY and itchy, repeated vaginal infections (yeast, loves glucose)
Complications of Diabetes Mellitus
D – drop in blood sugar (Hypoglycemia: less than 60 mg/dL)

I – increased risk of heart attacks and strokes (2–3 folds)
A – atherosclerosis ( hardening of vessels due to plaques)
B – blood pressure elevation & renal damage (nephropathy)
E – eye damage (retinopathy) & Diabetic maculopathy (central vision loss)
T – tingling, numbness, burning, or pinprick sensations. (NEUROPATHY)
E – early gum disease (tooth decay and carries)
S – sensorineural hearing loss (ear nerve damage)
Microangiopathy is specific to diabetes and most commonly affects the capillary membranes of
the eyes, kidneys, and skin nerves.
Macroangiopathy is a macrovascular damage a condition similar to atherosclerosis which
affects the large arteries (brain, heart & extremities).
LIFE THREATENING COMPLICATIONS
TYPE 1 DM — DKA
 DKA (Diabetic Ketoacidosis)
 MORE COMMON in Type 1 diabetics (rare to happen in type 2)
 There is NO insulin in the body and the body starts to burn fats for energy
 Due to this the ketones (KETO ACIDS), start to enter into the body and this causes life-
threatening situation, METABOLIC ACIDOSIS
 characterized by hyperglycemia, ketosis, acidosis, and dehydration
 Signs and Symptoms of DKA: N&V, excessive thirst, hyperglycemia, KUSSMAUL
breathing (air hunger, heavy labored breathing)
MANAGEMENT
A – Airway, Breathing and Circulation and Analysis
C – Commence fluid resuscitation:
T – Treat potassium
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R – Replace Insulin
A – Acidosis management
P – Prevent complications
I – Investigate (Monitor) therapy
D – Discharge:
A – Airway, Breathing and Circulation and Analysis: Stabilize and Send blood for metabolic
profile before initiation of fluids)
C – Commence fluid resuscitation:
 Initial fluid therapy: 0.9% NaCl (NS) 1 L/hour (15-20 ml/kg) in 1st hour and until
resolution of severe volume depletion
T – Treat potassium: Aim: K+ 3.3 to 5.3 mEq/L
 Withold insulin therapy until K+ >3.3 mEq/L or stop insulin whenever K+ <3.3 mEq/L
 Whenever K+ <5.3 mEq/L and adequate urine output of >50 ml/hour, 20 to 30 units
(mEq) of K+ should be added to each liter of infusion fluid
R – Replace Insulin:
 Initiate insulin only after giving 1 L NS over 1 hour and correcting K+ to >3.3 mEq/L
A – Acidosis management:
 In adult patients with pH <6.9, it is recommended that 100 mmol sodium bicarbonate in
400 mL sterile water (an isotonic solution) with 20 mEq KCl be administered at a rate of
200 mL/hour for 2 hours until pH >7.0.
P – Prevent complications: dehydration, hypovolaemia, hypotension, electrolyte
abnormalities, cardiac arrhythmias, cardiac arrest and cerebral edema.
I — Investigate (Monitor) therapy: serum glucose (every hour), electrolytes, calcium
magnesium and phosphate (every 2 hours), BUN, creatinine, ketones every 2 to6 hours)
D — Discharge: aim is to discharge the patient with sufficient education to prevent re-
admission with DKA in the future.
TYPE 2 DM — HHNS/HHNKS
 Hyperglycemic, Hyperosmolar, Nonketotic Coma
 Hyperglycemic hyperosmolar nonketotic syndrome
 OCCURS mainly in Type 2 diabetics
 Hyperglycemia without the breakdown of ketones
 Characterized by extreme hyperglycemia (600 - 1200 mg/dl or higher)
 Sufficient INSULIN is in the body to prevent ketones build up (prevents fat
breakdowns)
 NO acidosis/ketosis
 Signs and Symptoms of HHNS: VERY DEHYDRATED, thirsty, hyperglycemic,
mental status changes
Diabetes Nursing Management

Nurse’s role: educating, monitoring, and administering (medications)
Teach patient to follow the Triangle of Diabetes Management
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**Diet, medications, and exercise all work

together while monitoring blood glucose
Example: Patient wants to make sure their diet is balanced with their medication (insulin/oral
meds) and they use exercise to manage glucose levels (doing all this while monitoring blood
glucose).
As the nurse you will be educating the diabetic patient about:
 Diet, exercising, oral medications, giving insulin (peak times), drugs that increase
blood glucose and lower glucose etc.
Diabetic Diets
DIET: Diets are individualized due to physical activity and medication therapy (they always need
tweaking)…recommend following American Diabetic Association Diet (ADA)
Limitation of the following:
 Carbs (45-60%) grains, vegetables with starches potatoes, corn, sweets…
cookies, soda, dried beans, milk)
 Fats (<20 %)….limit unhealthy fats saturated, trans fats, cholesterol: lard, gravies,
whole milk, bologna, hot dogs, sausage, processed foods hydrogenated oils…
concentrate on mono & polyunsaturated avocadoes, olives, peanuts, nuts
 Proteins (15-20%) meats don’t increase the glycemic index: meats chicken,
turkey, fish, plant based beans, peas, low fat cheese, eggs whites
Exercising Management
Exercise: Aerobic the best (helps the body use insulin) ex: cardio running, walking, swimming
etc.
Teach patient signs of hypoglycemia & hyperglycemia
Signs of Hypoglycemia:
 “I’m sweaty, cold, and clammy….give me 5 hard candy”
o “Sweating, clammy, confusion, light headedness, double vision,
tremors, hunger, tired”
HYPERGLYCEMIA — “Hot and dry, sugar is high”

Signs of Hyperglycemia: Three P’s
 Polyphagia
o I’m hot and dry…My sugar is high!
 Polydipsia
 Polyuria
 Always check blood sugar prior to exercising: if lower than 100 eat a small carb
snack and carry SIMPLE carbs with you while exercising in case of hypoglycemic
attack
o Example of simple carbs: hard candy, honey, crackers/graham
crackers, fruit juice
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****If patient plans on exercising for an extended period of time, check glucose prior, during, and
after.
****If blood glucose is higher than 250 with ketones present in urine prior to exercise avoid
exercise until glucose and ketones stabilize.
Diabetic Medications
Oral medications (for patients with Type 2 diabetes when exercise and diet doesn’t work to
control blood glucose):
 Sulfonylureas: ides zides, mides, rides” (most common) stimulate beta cells in
pancreas to make insulin (Glyburide, Glipizide, Diabinese, Amaryl) AVOID
ETOH….extreme hypoglycemia
 Meglitinides: “glinide” Ex: repaglinide “Prandin” stimulate beta cells in pancreas to
make insulin…instruct pts to take first bite with meal
 Biguanides: Metformin (Glucophage)….causes the liver to decrease its stores of
glucose. Watch out if patient is scheduled for surgery/procedure (heart cath)…
stop for 48 hours and watch renal function…diarrhea
 Alpha-glucoside inhibitors: Precose, Glyset lower blood sugar by slowly down
the breakdown of starchy foods in the GI system which helps slowly rise the blood
sugar… instruct pts to take first bite with meal
 Thiazolidinedione: “glitazone” reduce glucose production in the liver:
Actos/Avandia watch liver function and heart function increase risk of MIs
Medications that cause hypoglycemia
 Remember from the hypertension lecture that Beta Blockers (mask symptoms of
hypoglycemia)
 Other medication that cause it: ETOH, ASA, Sulfonylureas (medications used to
treat type 2: Glyburide, Glipizide, Diabinese), and MAO inhibitors (meds for
depression) , Bactrim (common antibiotic)
Medications that cause hypergycemia
Thiazide diuretics (HCTZ), Glucocorticoids (Prednisone, Hydrocortisone), estrogen therapy
Insulin
It is used for Type 1 regularly, and sometimes for Type 2 diabetics if the patient is
experiencing stress on the body like surgery or illness.
Know the categories of insulin. Example: whether they are rapid, short, intermediate, long acting
and the onset, peak, and duration.
Note: Peak is the most susceptible time for hypoglycemia
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Key Points to Remember about Administering Insulin

 Rotate sites: do not use the same site more than once in a 2-3 week period this
PREVENTS LIPODYSTROPHY (pitting of subq fat)
o Sites include: abdomen, arms, and thighs
 When mixing insulin (clear to cloudy) clear=regular, cloudy=NPH
 Don’t massage site after administration increase hypoglycemia due to absorption
Mixing insulin steps

1. Inject air into cloudy insulin (intermediate-NPH)
2. Inject air into clear insulin (short-regular)
3. Draw up clear insulin (short– regular)
4. Draw up cloudy insulin (Intermediate– NPH)
*cloudy, clear, clear, cloudy
When mixing insulin, draw-up the into the syringe shorter-acting insulin, first & then the longer-
acting insulin
reduces risk of introducing the longer-acting insulin (cloudy) into shorter-acting (clear) insulin
vial & alters its action *clear over cloudy
Injections sites for insulin administration

 -abdomen (fastest speed of absorption)
 -upper arm (posterior surface) (faster)
 -thighs (anterior surface) (slow)
 -hips (slowest speed of absorption)
Systematic rotation of injection sites within an anatomic area is recommended to prevent:
localized changes in fatty tissue (lipodystrophy)
If pt is planning to exercise, insulin should not be injected into the limb that will be exercised
because this will cause the drug to be absorbed faster & may cause hypoglycemia
Example: bicycling, jogging, running DO NOT USE THIGH, USE ABDOMEN
Self-injection of insulin:
step 1 — With one hand, stabilize the skin by spreading it or pinching up a large area
step 2 — Pick up syringe w/other hand & hold it as you would a pencil. Insert needle straight
(90% angle) into skin.
step 3 — To inject the insulin, push the plunger all the way in.
step 4 — Pull needle straight out of skin. Press cotton ball over injection site for several
seconds.
step 5 — Use disposable syringe only once & discard into hard plastic container (w/tight fitting
tip) such as an empty bleach or detergent container. Follow state regulations for disposal of
syringes & needles.
Complications of insulin therapy

 Local allergic reactions
 Insulin lipodystrophy
 Systemic allergic reactions
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 Resistance to injected insulin

 Morning hyperglycemia
1) Local allergic reaction to insulin: redness, swelling, tenderness, & induration or a 2-4 cm
wheal may appear at injection site 1-2 hrs after; reaction usually disappears with
continued use of insulin
2) Systemic allergic reaction to insulin : rare; immediate local skin reaction that gradually
spreads into generalized urticaria (hives); can be assoc. w/generalized edema or
anaphylaxis
3) Tx for systemic allergic reaction to insulin: desensitization with small doses of insulin
administered in gradually increasing amounts using a desensitization kit
4) Insulin lipodystrophy — refers to a localized reaction, in the form of either lipoatrophy or
lipohypertrophy, due to repeated use of an injection site and lack of rotating
5) Lipoatrophy — loss of subQ fat; appears as slight dimpling or more serious pitting of
subq fat
6) Lipohypertrophy — development of fibro fatty masses at injection site caused by
repeated use of an injection site; if insulin is injected into scarred areas, absorption may
be delayed
Dawn Phenomenon:
Watch for Dawn phenomenon (hence the name dawn…crack of dawn means the waking hours)
this is a time when the body will increase the blood sugar in preparation for waking. However,
when you have insulin problems (not enough of it) the increased blood sugar causes
HYPERGLYCEMIA
Typical time: 5am to 8 am
Treatment: may need a night time dose of NPH to counteract.
Somogyi Effect:
Somogyi effect (remember S in Somogyi for sleeping hours): This is a drop in blood sugar at the
hours of 2 to 3 am. This happens when the body releases hormones such as coristol,
catecholamines, growth hormones to increase the blood sugar. However, in diabetics the body
can’t cope with the increased blood sugar and the sugar will be elevated.
Treatment: Eat a bedtime snack….a dose of bedtime insulin will prevent it from dropping so low
or decreasing insulin amounts at night
Hypoglycemia — less than 70mg/dL

Sweating, tremors, and tachycardia, thirst, and anxiety are early signs of hypoglycemia
TIRED
T-Tachycardia and Tremors (Shakiness)
I-Irritability and Headache
R-Restlessness and confusion
E-Excessive Hunger and light headed
D-Diaphoresis / Depression
Treatment: Need simple carbs if they can eat, or if unconscious and for SURGERY under
NPO — give IV D50
Simple carbs include: hard sugary candies, 4 ounce or ¼ cup fruit juice or soda, graham
crackers, honey
CARDIOVASVULAR DISORDERS
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CORONARY ARTERY DISEASE

 Disorder of the arteries in the heart, typically related to Atherosclerosis (plaque)
 Atherosclerosis is an inflammation process in INTIMA that results in fatty lesions
(plaque build up).
 Atherosclerosis — the primary factor in the development of coronary disease.
 Arteriosclerosis causes the HARDENING of the arterial wall, resulting in a loss of
elasticity and distensibility.
 CAD is the most common heart disease and number one cause of death.
PRIORITY causative factors: Cigarette smoking and hyperlipidemia.
Nonmodifiable risk factors:

-A Age
-G Gender and Genetic predisposition
-E Ethnicity and Family history
Modifiable risk factors:

C Cholesterol level
H Hypertension
O Obesity
L Lack of Physical activity
E Elevated triglyceride levels
S Stress
T Tobacco smoking
E elevated Homocysteine level
R Risk is high for patient with DM
O Overweight
L LDL level
Six test to diagnose CAD (hint: 3Es and 3Cs)

E Electrocardiogram (EKG)
E Echocardiogram
E Exercise stress test — Measures your heart rate while you walk on a treadmill
C Chest x-ray — create a picture of the heart, lungs, and other organs of the chest
C Cardiac catheterization — Checks the inside of your arteries for blockage by inserting a thin,
flexible tube through an artery in the groin, arm, or neck to reach the heart
C Coronary angiogram — Monitors blockage and flow of blood through the coronary arteries
using x-rays to detect dye injected via cardiac catheterization
Type of diet for reducing risk of CAD: Low sodium, low fat diet
Physical fitness: exercise 30 minutes >5 days/week
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MYOCARDIAL INFARCTION (HEART ATTACK)
CAUSE: Coronary artery thrombosis — most common cause for myocardial infarction
 Blood clot (thrombosis) that forms inside a coronary artery, or one of its branches.
This blocks the blood flow to a part of the heart.
Most common SITE of MI: Left ventricle
RISK FACTORS
MODIFIABLE
S smoking — strong risk factor for MI
M metabolic syndrome (HIGH BLOOD PRESSURE, DIABETES MELLITUS)
O overweight/obesity
K keeping a high level of stress (Chronic life stress, social isolation and anxiety)
E Elevated serum lipid levels /cholesterol is one of the most firmly established risk
factors for CAD.
R reduction of activity (physical inactive)
NON MODIFIABLE
A age — Older adults (>65) are more likely to die of heart disease.
G genetics and gender — men
E ethnicity — whites, blacks
MOST COMMON SYMPTOM: CHEST PAIN — resulting from deprivation of oxygen to the
heart.
 The chest pain for MI is usually described as an elephant sitting on the chest or a belt
squeezing the substernal midchest, often radiating to the jaw or left arm.
 (squeezing, aching, burning, sharp, dull, crushing, described as "like an elephant in
my chest")
 Pain radiates to: neck, shoulder, and jaw and down the left arm;
Chest pain – most common symptom

Dyspnea is the second most common symptom, related to an increase in the metabolic
needs of the body during an MI.
Edema is a later sign of heart failure, often seen after an MI.
SIGNS AND SYMPTOMS
CHEST PAIN
 Pain is crushing substernal pain
 Pain may radiate to the jaw, back and left arm
 Pain may occur without cause, primarily early in the morning
 Pain is unrelieved by rest or nitroglycerin and is relieved only opioids
 Pain lasts 30 minutes or longer (30– 60 mins)
Others: Feelings of nauseated, diaphoresis, shortness of breath, epigastric feeling of

indigestion or fullness
DIAGNOSTIC TEST:
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1. 12-lead electrocardiogram (ECG) — remains the most immediately accessible and

widely used initial diagnostic in M.I.
First: Peaked T waves or 'hyperacute' T-waves (HATW) are seen in early stages
(STEMI)
Second: ST elevation — most indicative sign of MI
Third: negative T wave inversion and / or ST segment depression — MOST indicative
sign of ISCHEMIA and angina
Pathologic Q waves — sign of previous myocardial infarction, the only residual

ECG signs of Myocardial infarction, permanent marker
2. CARDIAC MARKERS
A. CREATININE KINASE — used as a sensitive but NON SPECIFIC test for M.I
Three types:
1. MM- major CK form found in skeletal muscles
2. MB found in cardiac muscle, small amount in skeletal muscle
3. BB- brain; the only CK present in CSF
TAKE NOTE: CK-MB first to increase after an acute myocardial infarction, NOT as
specific for cardiac injury. Because a small amount is found in skeletal muscle. CK-
MB is not a good test!!
CK MB
Rises: 3-12 hours after infarction.
Peaks: 12-24 hours
Return to normal: 36-48 hours (2 -3 days) after infarction
B. Cardiac troponins "gold standard" in identifying myocardial infarction and

ischemia (cardiac marker of choice)
1. Troponin I — found only in the myocardium, most SPECIFIC for myocardial

damage
FIRST LINE blood test to confirm MI
Troponin is a highly specific cardiac marker for the detection of MI
MOST sensitive and specific marker for M.I
DEFINITIVE test and INDICATIVE test for MI
Rises: 4-12 hours after the onset of MI
Peak at 10-24 hours
Return to baseline after 10-14 days.
2. Troponin II — elevated for the longest period after MI

Rises: 3 to 4 hours after the onset of damage
Remains elevated : 4 to 7 days (troponin I) or 10 to 14 days (troponin T).
TREATMENT
TIME – is the MOST IMPORTANT FACTOR For a successful treatment of an acute M.I.
 An MI will cause permanent irreversible heart muscle damage if not re-perfused
within 4 – 6 hours.
 The best time to treat a heart attack is within 1 or 2 hours after symptoms begin.
 Waiting longer means more damage to your heart and a lower chance of survival.
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PRIMARY INTERVENTIONS: MONASAT DOES NOT REPRESENT, the order of priority

intervention
M morphine — opioid analgesic to reduce pain and allay anxiety (10 to 15 mg SQ, give IV if
unrelieved)
O oxygen – first intervention or priority of care, given thru NASAL CANULA 2 -6 L/m
N nitroglycerin – first line treatment for angina, causes vasodilation to improve blood flow
A aspirin – prevents Thromboxane A2, prevents platelet aggregation (antithrombotic action.)
S sedatives – Valium, give rest to patient to limit size of infarction
A anticoagulants – prevents blockage to coronary artery, reduces heart muscle damage
T thrombolytic – to dissolve thrombus or blood clots, given within 4 - 6 hours of infarction
(Streptokinase), but NOT more than 12 hours.
Others: Beta-adrenergic blockers — protect the myocardium, helping to reduce the risk of
another infarction by decreasing myocardial oxygen demand.
MUST KNOWS!!!
A Administering supplemental oxygen to the client is the first priority of care.

T To decrease oxygen demand on the client's heart is the primary reason for Morphine
administration
A administer morphine or nitro after successful oxygenation
K keep patient in Semi-fowlers position
E explain that SEX is resumption can be, when they can walk 1 block or climb 2 flights of
stairs without symptoms or 7-10 days after an uncomplicated MI.
MOST COMMON COMPLICATION OF MI: CARDIAC ARRYTHMIAS (ventricular fibrillation)

caused by oxygen deprivation to the myocardium.
MI completely heals: 6 to 8 weeks
 A damage heart needs 6 weeks to heal.
COLLABORATIVE REFERRAL: Cardiac rehabilitation
ANGINA PECTORIS
Angina Pectoris — "Strangling of the chest" , it is caused by a temporary imbalance

between the coronary arteries' ability to supply oxygen and the cardiac muscle's demand
for oxygen.
CAUSE: myocardial ischemia.

Most common sign: CHEST PAIN
CHEST PAIN:
LOCATION: substernal chest pain (retrosternal or slightly to the left of the sternum)
ONSET: Quickly or Slow
RADIATION: left shoulder and left arm,
 The pain usually radiates to the, and may then travel down the inner aspect of the
LEFT ARM to the elbow, wrist and Fourth and Fifth fingers.
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 The pain may also radiate to the right shoulder, neck, Jaw or epigastric region.
DURATION: LESS THAN 15 minutes

 Angina usually last less than 5 minutes. However, attack precipitated by a heavy meal or
extreme anger may last 15 to 20 minutes.
SENSATION: Clients describe the pain of angina as squeezing, burning, pressing, choking,
aching or bursting pressure. The clients often says the pain feels like gas, heart burn, or
indigestion.
SEVERITY: The pain of angina is usually mild or moderate in severity. It is often called
"discomfort", not "pain".
PRECIPITATING FACTORS:
S Smoking (Cigarette smoke) and caffeine ingestion
T Temperature (hot, humid environment; cold weather)
R Risk person are those with thyrotoxicosis
E Exertion (physical activity) or Stress (emotional stress)
S Severe anemia, fever, large meals
S Smog and high altitudes
CLINICAL MANIFESTATIONS
A abating pain or subsides with rest or nitro — important manifestation of angina
N nausea and vomiting, diaphoresis and pallor
G getting dizzy, lightheadedness, and syncope
I increase HR (Tachycardia or Palpitation)
N numbness or feeling of weakness in arms, wrist and hands
A anxiety, feeling of indigestion to a choking or heavy sensation in the upper chest
TYPES OF ANGINA
1. STABLE
 the most common type of angina
 result of myocardial ischemia and atherosclerosis
 Stable angina is a predictable pattern of chest pain.
 other terms for stable angina: chronic, classic, exertion angina
 triggered by one of the 4 E's: Exercise, Emotion, Exposure to cold, Eating
 more common in women, diabetic patients and the elderly.
 Increased demand, such as in physical activity, emotional stress, or excitement..
 characterized by a short-lasting burning, heavy, squeezing feeling in the chest.
 This type of angina is relieved by Nitroglycerine or rest.
2. PRINZMETAL/VARIANT
 chest pain that occurs as a result of coronary vasospasm.
 Most often occur same time each day, early morning
 reversible ST segment elevation in ECG
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 occurs primarily at rest and is triggered by smoking and increased levels of histamine
and epinephrine.
 signs and symptoms : syncope, dyspnea, palpitation
 generally responds to Nitroglycerin and Calcium channel blockers.
3. UNSTABLE ANGINA
 this type is classified between stable angina and MI.
 chest pain occurs with increased frequency, duration and intensity
 precipitated by progressively less effort
 any episode longer than 20 minutes, any new-onset angina, any increasing
(crescendo) angina, or even sudden development of shortness of breath
 the symptoms are NOT relieved by nitroglycerine.
 May progress to MI
4. MICROVASCULAR ANGINA
 is triggered by activities of daily life and exertion.
 occurs in the absence of coronary atherosclerosis or vasospasm.
 mainly associated with abnormalities of coronary microcirculation.
5. NOCTURNAL ANGINA – occurs at night, during sleep.
DIAGNOSTIC TEST
1. ECG - a depressed ST segment or inversion of the T wave, stop the test
immmediately. Show an association with an MI.
2. Exercise Stress Test - a depressed ST segment while exercising and hyportension,
stop the test.
3. Stress Echocardiagrm – A way to INDUCE CONTROLLED STRESS on the heart and
monitor its response (indicated for unstable angina)
4. Coronary Angiogram/arteriogram
 detect coronary artery spasms, check post-op pulses
 an invasive diagnostic study of the coronary arteries, heart chambers, and
function of the heart.
 Physician must obtain informed consent
 the femoral or radial artery will be accessed during the procedure.
 requires NPO for 6-12 hours prior to the procedure
 have an IV line started for sedation medications
 The client may feel warm and flushed while the dye is being injected.
 Compression is applied to the puncture site
 The client is required to lie flat for several hours following the procedure to
achieve hemostasis at the access site (femoral access).
 The client typically goes home the same day unless other interventions have
been performed
5. CARDIAC CATHETERIZATION
Pre-op
 PHYSICIAN must Obtain informed consent.
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 Assess for allergies to seafood, IODINE, or radiopaque dyes; if allergic, the client may
be premedicated with antihistamines and corticosteroids to prevent a reaction.
 Assess renal status
 Metformin (Glucophage) needs to be withheld 24 hours before and for 48 hours
after cardiac catheterization to prevent lactic acidosis
 NPO for 8 hours
 Document the client's height and weight (needed to calculate amount of dye needed)
 Document VS and assess distal peripheral pulse quality for post-op comparison
 Advise that a local anesthetic will be administer, may fell fatigue from prolonged lying,
may have desire to cough or a flush feeling when a catheter is inserted
Post-op
 Monitor VS and cardiac rhythm, notify MD for chest pain
 Monitor peripheral pulses and the color, warmth, and sensation of the extremity
distal to the insertion site at least every 30 minutes for 2 hours initially.
 Notify MD if there’s numbness and tingling, if the extremity becomes cool, pale, or
cyanotic, or if loss of the peripheral pulses occurs.
 Monitor for bleeding, hematoma; notify MD and sensitivity to the dye, risk for
pulmonary embolism
 Apply a sandbag or compression device (if prescribed) to the insertion site to provide
additional pressure if required.
 Keep extremity extended for 4 to 6 hours, keeping the leg straight to prevent arterial
occlusion (Femoral Access).
 Maintain strict bed rest for 6 to 12 hours. The client may turn from side to side. Do not
elevate the head of the bed more than 15 to 30 degrees.
 If the antecubital vessel was used, immobilize the arm with an armboard.
 The client is placed in the supine position and the head of the bed is not elevated
to more than 30 degrees to keep the affected leg straight at the groin and prevent
arterial occlusion.
 Bathroom privileges are not allowed during the immediate postcatheterization period.
 Encourage fluid intake to promote renal excretion of the dye and to replace fluid
loss caused by the osmotic diuretic effect of the dye.
 Infection may not be seen till 4 to 7 days (bacteria need multiply first)
 No heavy lifting (No more than 5 pounds)
Pharmacologic Treatment
 Nitrates are the mainstay for treatment of angina.
 Nitrostat or nitroglycerin is a vasoactive agent and it is administered to reduce
myocardial oxygen consumption, which decreases ischemia and relieves pain.
 Usual routes are SUBLINGUAL, as a spray, topical or I.V.
 nitroglycerin bottle is an amber color to maintain potency of drug, Because light
causes medication to deteriorate faster, vials are often amber to protect the contents
from the destructive effects of sunlight and artificial light.
 A burning sensation felt with sublingual forms indicates that the drug is still potent
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 Discard parenteral IV solution that is blue, green, or dark red
Nitrates
N Note: before giving a patient a nitrate ASK if they have taken Viagra or Cialis in past 24
hrs. Both have vasodilating effects resulting in SEVERE HYPOTENSION
I if the chest pain or discomfort is not relieved in 5 minutes after 1 dose, the patient (or family
member) should call 911 immediately.
T take 1 tablet under the tongue every 5 minutes up to 3 tabs for relief of pain- if no relief
refer
R refrain moving, Stop activity and sit or lie down, and take a sublingual tablet
O opened bottle of nitroglycerin should be replaced every 3 to 6 months
Nursing implications for Nitroglycerin

 instruct patients in proper technique and guidelines for taking sublingual nitroglycerin for
anginal pain
 NEVER chew or swallow the sublingual form
 Keep a fresh supply of sublingual medication on hand; potency is lost in about 3
months after the bottle has been opened
 To preserve potency, medications should be stored in an airtight, dark glass bottle
with a metal cap and no cotton filler
 Instruct patients in the proper application of nitrate topical ointments and transdermal
forms, including site rotation and removal of old medication
 To reduce tolerance, the patient may be instructed to remove topical forms at
bedtime and apply new doses in the morning, allowing for a nitrate-free period
 Take prn nitrates at the first hint of anginal pain
 NO DRIVING if under this medication
CONGESTIVE HEART FAILURE

 Congestive heart failure is the syndrome in which the heart has a reduced ability to fill
or pump blood,
 More than half of those who develop CHF die within 5 years of diagnosis.
MOST common cause of Left-Sided Failure: hypertension and aortic or mitral valve disease.
Right-Sided Failure common causes: pulmonary valve stenosis, emphysema and
pulmonary hypertension secondary to pulmonary emboli.
Congestive Heart Failure: Additive classification
DIAGNOSTIC TEST
ECHOCARDIOGRAM — CONFIRMS the diagnosis of heart failure
1. Left sided heart Failure

 the most common form of heart failure
 Left sided HF results from left ventricular dysfunction.
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 decreased functioning of the left ventricle. If left ventricular failure is significant, the
amount of blood ejected from the left ventricle drops greatly, resulting in decreased
cardiac output.
 As the left ventricle continues to fail, blood begins to pool in the pulmonary circulation,
causing pulmonary congestion.
AUSCULATED LUNG SOUND: CRACKLES — moist, gurgling noisy respirations

AUSCULTATED HEART SOUND: S3 (Systolic HF) & S4 (Diastolic HF)
Earliest sign— dyspnea upon exertion
CLINICAL MANIFESTATIONS (LEFT SIDED)
DROWNING
D Difficulty breathing (SOB) and restlessness

R Rales (crackles) — pulmonary congestion or edema
O Orthopnea, cool pale skin
W Weakness (due to shortness of breath)
N Nocturnal Paroxysmal dyspnea
I Increased heart rate (due to fluid overload)
N Nagging cough (can be frothy pink or blood-tinged sputum)
G Gaining weight (2 to 3 lb in a day or 5 lbs in a week)
Right Sided heart failure

 Right ventricle fails to contract effectively
 right sided heart failure causes a backup of blood into the right atrium and venous
circulation.
 primary cause of heart failure is left sided heart failure.
 may result from an acute condition such as right ventricle infarction or pulmonary
embolism.
 Cor Pulmonale (right ventricular dilation and hypertrophy caused by pulmonary
disease) can also cause right sided HF.
 pulmonary heart disease "cor pulmonale" as a complication from pulmonary
hypertension or COPD.
CLINICAL MANIFESTATION
SWELLING
S Swelling of legs, hands, liver,spleen abdomen
W Weight gain, anorexia, nausea and vomiting
E Edema (pitting) – dependent peripheral edema
L Large neck veins (jugular venous distention)
L Lethargic (weak and very tired)
I Irregular heart rate (atrial fibrillation)
N Nocturia
G Girth of abdomen increased (ascites)
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PRIORITY diagnosis the client with heart failure: impaired gas exchange related to inadequate
cardiac pump function.
HF with Pulmonary edema priority Nursing diagnosis — Activity intolerance related to
pump failure
Best position for the nurse to place the client in when observing for JVD: Head of the
bed elevated to a 30 to 45-degree angle
 Report if 4cm above sternal angle
Pitting edema assessment (based on the depth and duration of the indentation).
1+ mild, slight indentation, no perceptible swelling;
2+ moderate pitting, indentation subsides rapidly;
3+ deep pitting, indentation remains, leg looks swollen
4+ very deep pitting, indentation lasts long time, leg very swollen
The main goal in the treatment of chronic HF is

 to treat the underlying cause and contributing factors
 PREVENT EXACERBATIONS
 maximize CO
 provide treatment to alleviate symptom
 improve ventricular function
 improve quality of life
 preserve target organ function
 improve mortality and morbidity.
MEDICATIONS
1. Lisinopril (ACE inhibitor) — improve client symptoms as well as increase survival
2. Metoprolol (Beta adrenergic blocker) — Usually begin after ACE inhibitor & diuretics
have been stabilized for 2 weeks (Monitor & hold for hypotension & bradycardia)
3. Digitalis glycosides (Lanoxin) — remain the mainstay in the treatment of HF
 Increases contractility (+inotropic)
 Reduces heart rate (– chonotropic)
 Decreases electrical conduction(negative dromotropic)
 CHECK HR, Hold if below 60 and above 100
 CHECK K+ level (hold if <3.5mEqs), HYPOKALEMIA increases toxicity
 Mild diuretic effect — INCREASED URINE OUTPUT suggest drug is effective
 Therapeutic levels are 0.5-2.0 ng/ml. A serum digoxin level >2.0 ng/ml can indicate
digitalis (digoxin) toxicity.
 signs and symptoms of early/mild digoxin toxicity: G.I. issues are the #1 first sign of
early toxicity (NV) anorexia fatigue nausea vomiting or changes in mental
status
 yellow/green halos or visual disturbances and cardiac dysrhythmias
 Digifab — antidote used for digoxin toxicity
 Contraindications of digoxin: drug allergy, second or third degree heart block
ventricular fibrillation
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HEART FAILURE CONSIDERATION

F fowlers position for DOB and pulmonary edema
A Auscultate breath sounds q1-4 hrs
I impaired gas exchange — PULSE OXIMETER, Administer prescribed O2 (2L/min)
L limit fluid intake to 2,000 mL/day, limit Na 2-3g/day, avoid saturated and transfat
U use furosemide diuretic, to mobilize edema, pulmonary venous pressure, and reduce preload.
R Reinforce HTN, DM control, obesity, smoking
E Encourage rest and activity alternations to preserve energy
Three most common complications of Heart Failure

- arrhythmias:
- pulmonary edema: backflow from left ventricle to lungs
- cardiogenic shock
Peripheral Arterial Disease — term used to describe a wide variety of conditions affecting
arteries in neck, abdomen, and extremities
PAD risk factors: High cholesterol, diabetes mellitus, uncontrolled hypertension, and smoking
PVD risk factors: Pregnancy, being female, varicose veins are risk factors for peripheral
venous disease.
◾Atherosclerosis is the most common cause of PAD (peripheral arterial disease). This is the
collection of fatty plaques on the artery wall. This blocks blood flow.
◾intermittent claudication and is a HALLMARK sign and symptom in PAD.
◾PAIN most commonly occurs at night and can wake up the patient. It is known as “rest
pain”.
Buerger's Disease / Thromboangitis Obliterans
OTHER NAMES OF BUERGER'S DISEASE:

 THROMBOANGITIS OBLITERANS
 INTERMITTENT CLAUDICATION
 CHILLBLAINS
BUERGERS DISEASE
- INFLAMMATORY occlusions of DISTAL ARTERIES AND VEINS - Relatively uncommon
- MEDIUM and SMALL arteries and veins are affected
– MOST common in DISTAL LOWER extremities and DISTAL UPPER LIMBS
RISK FACTORS
1. Young MEN
2. 20-45 years of age
3. Smokers – GREATEST RISK FACTOR
4. Cause is UNKNOWN may be genetic or autoimmune
55
MANIFESTATIONS (S/Sx):
MOST common symptom: PAIN with exercise affecting the arch of the foot (instep Claudia
Timon.)
1. Intermittent Claudication (pain): pain in muscles from low blood supply of the arch of the
foot – FIRST SIGN: intermittent claudication may occur in LOWER extremities
◾Intermittent claudication is a dull, tight, aching, or squeezing pain in the calf, foot, thigh, or
buttock that occurs during exercise, such as walking up a steep, that can be ISUALLY
RELIEVED BY REST.
2. Aching pain: excruciating

3. Tingling and numbness — COLDNESS/NUMBNESS/TINGLINGING/ BURNING
4. Persistent coolness — Skin of foot is COOL, THIN, INELASTIC with no hair growth on
dorsum of toes
5. Reduced or absent arterial pulses/diminished distal pulses (dorsalis pedis)
6. Sensitivity to COLD
7. reddened or cyanotic extremities in dependent position
8. may have ulcerations or gangrene of the digits
9. Pitting edema at the END OF THE DAY
10. GANGRENE
SYMPTOM'S of BUERGER'S DISEASE

o COLD FEET (white, blue, red, tingling/prickly)
o INTERMITTENT CLAUDICATION (cramping pain in calf/foot)
o Progression= Pain comes sooner & subsides more slowly
o LA REICH SYNDROME- intermittent claudication felt as cramping/aching in
buttocks, implies arterial
Major complication: CLOTS
Buerger's management
1. Stop smoking (smoking cessation), nicotine replacement products should not be used
2. Vasodilator drugs:trental
3. Low dose ASA - breaks clots, prevents clots
4. Keep warm, avoid cold - vasodilation
5. Foot care: prevent trauma to feet (must avoid)
6. Monitor peripheral pulses frequently
7. May need arterial bypass surgery/amputation
priority to educate the patient on smoking cessation.
RAYNAUDS DISEASE
 Episodic VASOSPASM of the SMALL CUTANEOUS ARTERIES,
 COMMON IN: fingers and toes sometimes ears, and cheeks
 Primarily seen in: YOUNG WOMEN
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CAUSE: UNKNOWN
RISK FACTORS
 Females
 Family history
 Age <30 years old
 Injury to hands
 Living in cold environment
 Repetitive use of hands
 Occupational exposure to certain workplace chemicals
 Smoking
SECONDARY RAYNAUDS PHENOMENA – occurs in association c autoimmune disorders
(RA, scleroderma, or lupus),
MANIFESTATIONS
1. Swelling
2. Throbbing
3. Numbness, tingling, swelling, and cold temperature at the affected body part
4. Paresthesia — a tingling, pricking, chilling, burning, or numb sensation on the skin)
especially upon warming or stress relief
5. Changes in skin color (WHITE –> BLUE—>RED)
Three phases:
1. Pallor (white)-due to decreased or absent blood flow
2. Cyanosis (blue)-due to capillary dilation distal to vasospasm
3. Rubor (red)-due to excessive reactive vasodilation
TAKE NOTE: Attacks are intermittent and occur with exposure to cold or stress
Raynaud's Disease management

* Stop smoking
* Avoid cold, stress, keep warm
* Protect hands from injury, wounds heal slowly
* Vasodilator drugs
MEDICATIONS
1. Calcium channel blockers (Nifedipine)
2. Nitrates (transdermal or oral)
3. Aspirin - to decrease platelet aggregation
Complications of raynaud's includes

 Ischemia
 Gangrene
 Arterial ulcers
 Limb amputation
General Tx
 Local warming measures slowly to prevent shock
 Smoking cessation
57
 Use of gloves or insulating clothing layers to keep warm

 Avoidance activities and places involving exposure to cold and mechanical or chemical
injury
 Avoid stressful environments
ONCOLOGY NURSING
Cancer is a generic term for a large group of diseases that can affect any part of the body.
Other terms used are malignant tumors and neoplasms
 Cancer is the second leading cause of death globally
6 hallmarks of cancer:
1. Sustained proliferative signaling
2. Evading growth suppressors
3. Activating invasion and metastasis
4. Enabling replicative immortality
5. Induces angiogenesis
6. Resist cell death
Most prominent cancer hallmark, i.e., 'sustaining proliferative signaling'.
Carcinogens – cigarette smoke, viruses that cause chronic infection of the liver and the uterine
cervix, hormones such as estrogen, and ultraviolet rays from the sun.
The major promoters of health are healthy diet, physical fitness and possibly less stress.
Incidence of cancer increases with increasing age.

LOWER rate in Children
HIGHEST rate 65 years old above
Cancer survival usually 5 or 10 years

More FEMALES may live up to age 75
More MALES may die before age 75
The major factors involved in the causation of cancer, as well as many other chronic
degenerative diseases, are :
 CIGARETTE SMOKING, UNHEALTHY DIET, ALCOHOL DRINKING, PHYSICAL
INACTIVITY, OBESITY, HORMONES, VIRUSES, and IONISING RADIATION.
MUST KNOWS
1. Cancer protecting mechanisms prevent cancer. A healthy lifestyle that is started in
childhood, particularly eating a HEALTHY DIET, maintaining PHYSICAL
2. FITNESS and MINIMIZING/ PROPERLY COPING with STRESS may decrease the risk
of cancer, coronary artery disease, hypertension, stroke and diabetes.
3. Healthy diet is low in animal fat, rich in starchy foods (such as cereals, tubers and
pulses), with substantial fruits and vegetables.
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4. Unhealthy diet is rich in fat, salt and free sugars, and/or in smoked, salt-pickled/-
preserved foods.
5. Cigarette smoke is the most pervasive cancer causing substance.
6. The numerous carcinogenic agents found in cigarette smoke cause cancers of the lung,
mouth, pharynx, larynx, esophagus, other cancers, and other acute and chronic
diseases.
7. High alcohol consumption also increases the risk of many cancers.

8. Betel-quid chewing causes cancer of the mouth
9. Hepatitis B virus (HBV) is the most common cause of liver cancer in the Philippines.
10. Human papilloma virus (HPV) causes cancer of the uterine cervix and is transmitted
through sexual intercourse.
11. Ultraviolet rays from the sun are capable of causing skin cancer, particularly in fair-
skinned persons.
12. Majority of cancers can be cured if they are detected early.
13. NOT all cancers can be detected early enough to be cured.
14. Surgery is currently the most effective and widely accessible form of treatment for
majority of cancers that can be cured if detected early.
15. These common cancers can be detected early and when treated properly can be cured -
BREAST, CERVIX, COLON, RECTUM, ORAL, THYROID, PROSTATE.
9 WARNING S/sx of CANCER "CAUTION US"
C: Change in bowel or bladder habits.

A: A sore that does not heal.
U: Unusual bleeding or discharge.
T: Thickening or lump in the breast or elsewhere.
I: Indigestion or difficulty in swallowing
O: Obvious change in a wart or mole
N: Nagging cough or hoarseness.
U: Unexplained anemia.
S: Sudden weight loss.
IARC-GLOBOCAN facilitates national estimation of cancer incidence every 5 years
Carcinogenesis
 process of transforming normal cells into malignant cells
Three phases of cancer development.
1. Initiation
—FIRST phase of carcinogenesis
—Initial DNA mutation occurs
—Irreversible step in malignant transformation
Hallmark: DNA Damage
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2. Promotion
— REVERSIBLE stage of cancer
— proliferation of the altered cells.
3. Progression
— IRREVERSIBLE and FINAL stage of cancer
— can lead to METASTASIS
— Chromosomal abnormalities are present
1. Breast Cancer
Breast cancer is the leading site for both sexes combined (19%) in 2015 and ranks 1st
among women (33%).
RISK FACTORS:
B being a Female
R reproductive age: early menarche before 12 and late menopause, NULLIGRAVIDA by age
35 or 1st child after age 30
E estrogen and diethylstilbestrol (DES).
A alcohol use
S smoking cigarette
T treatment history (HRT, RADIATION)
Moderate risk factor: high fat diet, obesity, having dense breast
Significant risk factors: Family history or previous cancer treatment history
LOWER RISK: Women who have had children and BREASTFEEDING
BRCA - Lifetime risk of breast cancer:
BRCA1 36-87%
BRCA2 45-84%
TAKE NOTE: Alcohol is the best established dietary risk factor for breast cancer, probably
by increasing endogenous estrogen levels.
SIGNS & SYMPTOMS
M – Mass or lump which is PAINLESS (Main Sign)

A – Axillary nodes involvement (most important prognostic indicator)
S – Serosanguinous or bloody nipple discharge (2nd most common)
S – Skin changes: Peau d'orange (late stage)
Peau d'orange
O – orange peel skin
R – red and warm skin (inflamed)
A – Around nipple rash: red crusty, scaly/flaky skin (Paget disease)
N – Nipple retraction & dimpling or puckering of skin (raise arms over the head)
G – getting tender , burning , sticking breast
E – enlargement of axillary nodes
SCREENING TEST:
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1. BREAST SELF EXAMINATION:
Breast self exam: MONTHLY starting at age 30

BEST TIME: 5 to 7 days after the first day of the menstrual period (POST
MENSTRUAL) when the breasts are the smallest and least congested
BEST TIME for postmenopausal women to perform BSEs is: On the same day every
month. (Convenient day to patient)
BEST POSITION: SUPINE LYING — nipple is pointing towards ceiling
BEST TECHNIQUE: Vertical strip pattern( up and down approach) — best
technique to detect masses
ASESSMENT TOOL: PALPATION TECHNIQIE – Use the flat pads of three fingers.
 In inspection it is common to have a slight asymmetry in size; LEFT
breast is slightly larger than the right
 Start palpation at the Upper outer quadrant
Supine palpation steps in order.

1. Help the patient lie down.
2. Place a towel under one shoulder.
3. Have the patient raise that arm above the head.
4. Make sure the nipples are pointed toward the ceiling.
5. Palpate each breast separately.
MOST COMMON SITE OF TUMOR: upper outer quadrant

NOTE: palpate also the axillary tail of Spence, the cone-shaped breast tissue that projects up
into the axilla, close to the pectoral group of axillary lymph nodes.
Lymph nodes that are responsible for drainage from the arms are the lateral lymph nodes.
BENIGN: MOBILE, WELL DELINEATED MASS

MALIGNANT: Single, firm, FIXED nodule
2. Clinical breast exam:

Age 20 to 39: EVERY 3 YEARS
At or After 40 y.o.: EVERY YEAR
3. Mammography
YEARLY(ANNUALY) — at age 40
Start at age 30 to 35 if with FAMILY HISTORY
PREEXAMINATON: Removal of deodorants, antiperspirants, powders, creams, lotions
and jewelry
 Powder, deodorant, and jewelry can distort the images on film as calcium spots and
should not be worn
 Should be scheduled JUST AFTER menses, when the breasts are the least tender.
 Mammograms are 5- to 10-minute procedure.
 Pain relievers, acetaminophen and ibuprofen may ease discomfort AFTER procedure
CONFIRMATORY: BIOPSY
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1. FNAB (Fine needle Aspiration Biopsy) take out a small amount of fluid and very small
pieces of tissue from the tumor, if the specimen is positive for malignancy, the patient
can be told at the visit.
2. LCNB (Large Core Needle Biopsy) sample of tissue retrieved using a large bore needle
(such as a tru-cut) for pathology.
The TNM system: Tumor, lymph Nodes, Metastasis
TNM
T = Tumor
N = Nodes
M = Metastasis
TUMOR
TX: The tumor size can't be measured
T0: N0 primary tumor, or it can't be found
Tis: Tumor is "in siTu," meaning it is small and completely contained in the tissue where
it started
T1 = lesion is <2 cm in size
T2 = lesion is 2-5 cm
T3 = skin and/or chest wall involved by invasion
NODES
NX: Nearby lymph nodes can't be tested or evaluated
N0: No cancer in nearby lymph nodes, or it can't be found (no axillary nodes involved)
N1 = mobile nodes involved
N2 = fixed nodes involved
N3 = means that cancer in the lymph nodes is extensive and widespread.
METASTASIS
MX: It's unknown if the cancer has spread
M0: Cancer has not spread to other parts of the body, or it can't be found anywhere else
M1: Cancer has spread to one or more distant parts of the body
STAGES
Stage 0 is used to describe non-invasive breast cancers, such as DCIS (ductal carcinoma in
situ). In stage 0, there is no evidence of cancer cells or non-cancerous abnormal cells
Stage IA – tumor measures up to 2 centimeters (cm) and the cancer has NOT spread
outside the breast; NO lymph nodes involved.
Stage II - tumor size up to 5 cm with axillary and neck lymph node involvement.
Stage III – tumor larger than 5 cm; cancer has spread to 1 to 3 axillary lymph nodes or to
the lymph nodes near the breastbone.
Stage IV – cancer that has spread beyond the breast and nearby lymph nodes to other
organs of the body, such as the lungs, distant lymph nodes, skin, bones, liver, or brain.
SURGERY: MASTECTOMY
INDICATIONS:
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1. Tumor involves the nipple-areola complex

2. Tumor is larger than 7 cm
3. Tumor exhibits extensive intraductal disease involving multiple quadrants of the breast
4. Patient cannot comply with daily radiation therapy
GOAL of breast cancer surgery: to remove the tumor itself and a portion of surrounding tissue
while conserving as much of the breast as possible.
TYPES
1. Simple or Total Mastectomy – removal of entire breast, and nipple, but NOT lymph
nodes
2. Modified Radical Mastectomy – removal of entire breast is removed, including the

skin, areola, nipple, and most axillary lymph nodes, but the pectoralis major muscle is
spared.
 Primary method of treatment for breast cancer
 Affected side should be elevated on pillows to help prevent the development
of lymphedema.
 On the day of surgery, the client should be encouraged to move the fingers and
wrists of the affected arm.
 Hair combing and wall climbing exercises will be performed later, not on the day
of surgery.
 Arm exercises are instituted gradually at the surgeon's direction with the goal of
returning to full ROM in 4 to 6 weeks, prevent CONTRACTURES & MUSCLE
SHORTENING.
 NO VENIPUNCTURES and BP taking in affected side. (To prevent
lymphedema)
3. Radical Mastectomy (Halstead surgery)– removal of entire breast is removed, including

the skin, areola, nipple, and most axillary lymph nodes, and pectoralis major muscle.
OUTDATED TERM, NEVER DONE ANYMORE
4. Skin-Sparing Mastectomy — all of the breast skin, except the nipple and the areola, is
preserved (for breast reconstruction)
5. Lumpectomy (Partial Mastectomy) – removal of a breast lump with a surrounding rim
of normal breast tissue. NEEDS RADIATION AFTER.
Multidisciplinary Approach for Breast Cancer Coordinate with other disciplines (chemo,
radiation)
Pharmacologic Therapy
1. Chemotherapy is the primary used as adjuvant treatment postoperatively ; usually
begins 4 weeks after surgery
 Treatments are given every 3 to 4 weeks for 6 to 9 months.
 Principal breast cancer drugs include cyclophosphamide, methotrexate,
fluorouracil, doxorubicin, and paclitaxel.
 Cyclophosphamide (Cytoxan) is a CELL CYCLE NONSPECIFIC DRUG
 Hemorrhagic cystitis is the potentially fatal side effect of Cytoxan.
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
Herceptin can lead to ventricular dysfunction, so the patient is taught to self-
monitor for symptoms of heart failure, ventricular dysfunction
 Tamoxifen (anti estrogen) is used for estrogen-dependent breast tumors in
premenopausal women.
RADIATION THERAPY:
1. External radiation for breast cancer lasts 5 to 6 weeks

2. Brachytherapy (internal radiation) last 1 to 5 days.
BRACHYTHERAPY – radioactive seed/pellet are inserted into a multicatheter or balloon

catheter device; given over 5 days; 10 total treatments; 6 hrs in between treatments
 patient may need to be in the hospital 1-2 days
 unsealed brachytherapy – temporary or permanent radiation source (lid implant) is

implanted with the tumor target tissue
 sealed brachytherapy – the client emits radiation while the implant is in place, but the
excreta are not radioactive
ALARA – As Low As Reasonably Achievable by time, distance, shielding

D – Distance: Stay at least 6 feet from source
T – Timing: limit time in room to max. of 30 minutes/ 8 hr. shift
S – Shielding: Wear lead apron, dosimeter film badge must be worn when in the client's room.
General considerations
R room patient in PRIVATE room, keep door close as much as possible (door warning sign)
A ages 18 below children and pregnant should not come in contact with the client or source
D Don't touch with bare hands, use long handled forceps to place source in lead container
I inspect all linens before discarding to make sure implant/ seeds have not been released
A all linens, gowns, dressings, equipment, trash in patient's room must be saved until patient
discharged.
T time and limit visitors to 30-60 minutes/ day, visitors should stay at least 6 feet from source.
I instruct nurses to wear mask, gown, gloves and dosimeter film badge when caring patient
O organize care so that nurse/ staff exposure is kept to a minimum
N never care for more than 1-2 radiation implant patients at a time.
Take note: Rotate assignments to minimize exposure, provide care on opposite side of implant
EXTERNAL RADIATION — Constipation is common

INTERNAL RADIATION — FATIGUE is common
PALLIATIVE CARE
Palliative care is about caring for people who have an illness that is not responsive to curative
treatment. The focus is not to cure but to 'palliate'- to relieve suffering
FOCUS OF PALLIATIVE CARE

1. Improve her quality of life.
2. Focus on reducing the severity of disease symptoms.
3. Meeting the patient's physiologic and safety needs is the priority.
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Specific goals of palliative care

 Regard dying as a normal process.
 Provide relief from symptoms, including pain.
 Affirm life and neither hasten nor postpone death.
 Support holistic patient care and enhance quality of life.
 Offer support to patients to live as actively as possible until death.
 Offer support to the family during the patient's illness and their own bereavement.
MUST KNOWS
 Freedom from cancer pain is essential to palliative care.
 The right drug in the right dose and route given at the right time will relieve cancer pain.
 Opioids do not cause addiction among patients treated for cancer pain. (use WHO
ladder)
 Strong opioids should not be withheld until the patient is dying.
 The prescription of strong opioids does not mean that death is near.
 An acceptable quality of life does not only involve cancer pain relief.
 The FAMILY is the unit of care in palliative medicine, and the HOME is the ideal
location of palliative care.
Three main principles of the WHO analgesic ladder

 By the clock, by the mouth, by the ladder
1. Mild Pain — Non-opioid analgesics (acetylsalicylic acid, acetaminophen, ibuprofen

and selective and non-selective NSAIDs)
2. Moderate pain – Weak opioids (codeine, hydrocodone, and tramadol)
3. Severe pain – Strong opioids (morphine, oxycodone, meperidine methadone,
hydromorphone, fentanyl, Levorphanol)
2. LUNG CANCER
RISK FACTORS
BIGGEST RISK FACTOR: Smoking cigarettes is the single biggest risk factor for lung
cancer. (80–90%)
Incidence increases with age: over 50 (Genetic predisposition)
L – Living close to banana plantation

U – Urban living (Air pollution)
N – Nanay (mother) cancer history or FAMILY HISTORY
G – Gas inhalation like RADON, ASBESTOS, mustard gas, arsenic, nickel, diesel
S – Sprayer of pesticides and exposure to ionizing radiation
TYPES OF LUNG CANCER

1. Small cell lung cancer (oat cell cancer)– least common type of lung cancer (10 -
15%) spreads faster.
2. Non-small cell lung cancer (NSCLC) – most common type (80% to 85%).
 Adenocarcinoma is the most common form.
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 Squamous cell carcinoma is the second most common type of lung cancer, typically
central, and the type most likely to cavitate and/or cause hemoptysis. Best prognosis
 Small cell carcinoma is the third typically central and already metastatic at presentation
SIGNS/SYMPTOMS:
EARLY WARNING SIGN: persistent, dry cough
D dry and persistent cough

R recurrent episodes of pneumonia
Y you may have Hemoptysis: Blood streaked sputum (rusty, purulent)
C Chest pain or chest tightness and DOB

O one or two signs plus fever
U unexplained weight loss and anorexia
G getting worst cough (2 to 3 weeks)
H hoarseness and dysphagia
DIAGNOSTIC TEST
1. Chest X-ray – 1st test used to diagnose lung cancer. Most lung tumors appear on X-
rays as a white-grey mass
3. NOT a definitive diagnosis
2. CT scan – next test after a chest X-ray. (Injection of dye)
3. PET-CT scan – done after CT SCAN shows cancer
4. PET-CT scan positron emission tomography-computerized tomography) can show
where there are active cancer cells. help with diagnosis and choosing the best
treatment.
5. Injection of radioactive meterial , scan is painless for 30 to 60 secs.
4. Bronchoscopy and biopsy
 Bronchoscopy shows detailed description of the tracheobronchial tree and allows
for biopsies of suspicious areas
 Percutaneous Biopsy — for confirmatory
Risks of biopsies: pneumothorax (air leaks out of the lung)

WOF: Sudden shortness of breath
offer an acceptable quality of life.
Treatment : Radiation therapy, chemotherapy, and surgical resection are all used in the
treatment of lung cancer.
KEY to increasing the survival rates of clients with lung cancer: EARLY DETECTION
SURGERIES:
1. WEDGE RESECTION – A small area of tissue close to the surface of the lung is
removed
2. PNEUMONECTOMY – An entire lung is removed (Chest tube is NOT required)
3. LOBECTOMY– a lobe is removed (Chest tube is NEEDED), one or more segment
(partial lobectomy)
4. SEGMENTAL RESECTION – A segment of the lung is removed
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POST OPERATIVE POSITIONING: “LU -PA”

PNEUMONECTOMY — Position on AFFECTED SIDE (surgical side down, good lung up)
AVOID severe lateral positioning --> mediastinal shift.
LOBECTOMY — lie on UNAFFECTED SIDE w/ HOB @ 45 degree
Terminal lung cancer intervention: Provide pain control

Signs and symptoms associated with metastatic lung cancer include: fatigue, bone pain,
Seizures
WOF
HORNERS SYNDROME — drooping eyelid and small pupil in the same eye, present when
there is a superior sulcus tumors
PANCOAST SYNDROME – shoulder, hand and arm pain present when tumor is at the very top
(apex) of the right or left lung
3. Colon-Rectum Cancer
 Most colorectal cancers start as a growth on the inner lining of the colon or rectum.
These growths are called polyps.
 Colorectal polyps are common with colon cancer.
Most common type: adenocarcinoma (95%) “apple-core" or "napkin-ring" like

Most common site: sigmoid colon
RISK FACTORS
C consumption of red and/or processed meat

O overweight or obese
L low-fiber and high-fat diet
O older than 50
R race and family history
E excess sugar consumption
C Crohn’s disease or ulcerative colitis.
T tobacco smoking
A alcohol consumption
L Lack of regular physical activity.
WARNING SIGN: change in bowel habits, such as alternating constipation and diarrhea
SIGNS/SYMPTOMS
C changes in bowel habit: alternating constipation & diarrhea (most common)
O overt blood in stool, melena and hematochezia (2nd most common)
L loss of weight(unexplained), Unexplained anemia, anorexia, weight loss, fatigue
O obstruction (abdominal pain and cramping, constipation, distention)
N narrowing of stools (ribbon like or pencil like stool) and tenesmus
Melena — RIGHT-sided colon cancer

Hematochezia — LEFT-sided colon cancer
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Early detection: At age 50, a colonoscopy, then once every 5-10 years.
Diagnosis
1. Stool for guiac – to test occult blood in stool (positive results turns blue or blue
green)
 Avoid in 3 days before test: BEEF & other red meats apples, broccoli, cauliflower,
turnips, parsnips, horseradishes, bananas, grapes cantaloupe (false positive result)
 Avoid in 7 days before test: NSAIDS and ASPIRIN ( to avoid gastric irritation)
 Avoid in 3 days before test: VITAMIN C and IRON with vitamin C (false negative
result)
2. CEA (tumor marker) – carcinoembryonic antigen (CEA) , small protein) that is found
on the surface of colon.
3. Barium enema – Barium enema with air contrast (to check for growth of tumor)
GoLytely would cause severe cramping and could cause an emergency.
Tap water enema is the way to clean out the pt before diagnostic testing.
Before test
 Low residue diet 1-2 days
 Clear liquid diet the night before
 Laxative will be given night before
 cleansing enemas the morning of the test(if there is no inflammation or bleeding)
up to
 3 could be given until solution is clear
 continue meds
During test
 Position – sims in left side
 proper sequence for filling the large intestine: Rectum, sigmoid, descending
colon, transverse colon, and ascending colon
After test
 Monitor passage of stool
 Stool will appear white, clay or gray in color until all barium has been
evacuated.
 Increase fluid intake after test to dilute barium and facilitate elimination.
4. Proctosigmoidoscopy — Examination of the rectum and sigmoid colon
5. Colonoscopy (with biopsy) —gold standard screening and the most sensitive
test used to detect colon cancer
 Colonoscopy uses a long, flexible and slender tube attached to a video camera
 Clear liquid diet the day prior to colonoscopy
 remaining NPO 8 hours before colonoscopy
 Bowel preparation: citrate of magnesia, laxatives, or polyethylene
 short procedure - 15- 20 minutes
 no sedation or anesthesia
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Definitive treatment for colon cancer: Surgery (Colectomy)

 Removal of polyp/tumor, surrounding colon, and/or lymph nodes by surgery or
colonoscopy
1. Right hemi-colectomy: for cecum and ascending colon cancer

2. Extended right hemi-colectomy: for transverse colon cancer
3. Left Hemi-colectomy: for descending colon cancer
4. Sigmoid colectomy: for sigmoid cancer
5. Anterior resection: for rectal cancer
CONSISTENCY OF STOOL
1. Ileostomy — WATERY to thick liquid (avoid eating Corn, popcorn, nut and seeds)
2. Ascending colostomy — liquid
3. Transverse Colostomy: thick liquid to SEMI-FORMED
4. Descending/Sigmoid: similar to normal solid consistency (SOLID FORMED stool), risk
for bowel continence
STOMA CARE
S shiny, wet, moist and red or dark pink in color (beefy red) is normal appearance
T treat skin irritation (Karaya powder), avoid soap
O Onions, alcoholic beverages, eggs, and cabbage must be avoided
M monitor signs of infection, necrosis, ischemia (purple, black, brown color)
A An edematous stoma is normal, edematous initially and shrinks over the next 4 to 6 weeks.
C changed pouch every 3 to 7 days, not daily

A after a fecal surgical diversion, Place a pouch over the newly created stoma
R report to MD if pale pink patient (may have a low hgb and hct)
E empty pouch when 1/3 to 1/2 full.
LIVER CANCER
 Malignant cells growing in the tissues of the liver
 Rapidly fatal, usually within 6 months if unresectable
 Second leading cause of fatal hepatic disease (after cirrhosis)
 The liver is one of the most common sites of metastasis from other primary cancers.
 Most primary liver tumors (90%) are hepatomas originating in the parenchymal cells.
 Survival year is 5 YEARS
1. Primary liver cancer – hepatocellular cancer

 more common in MEN with chronic liver disease.
 More common in developed countries
2. Secondary liver cancer – secondary liver cancer is much more common than primary
liver cancer
 metastatic liver cancer (colorectal, breast and lung)
Incidence: Men, more that 55 years old
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Most common risk factor: HBV and HCV infection

1. America– hepatitis C
2. Asia – hepatitis B
Risk Factors
L liver cirrhosis
I intake of alcohol, foods with AFLATOXIN, RED MEATS and saturated fats
V viral infection (chronic Hepa B and C)
E extra fat in the liver not caused by alcohol (non alcoholic fatty liver disease
R race: Asian and Pacific Islanders (highest rates of liver cancer), Black American
Others: DM, OBESITY, Wilson's disease, Autoimmune liver disease, Hemochromatosis

SIGNS/SYMPTOMS:
Warning sign: Epigastric or RUQ pain and unexplained weight loss
Early signs
Splenomegaly
Hepatomegaly
Ascites (increase abdominal girth)
Fatigue
Peripheral edema
Portal hypertension
Late signs
Anorexia
Weight loss and cachexia
Fever/chills
Jaundice
Palpable mass
Right upper quadrant tenderness dull abdominal pain in epigastric
DIAGNOSTIC TEST
1. Alpha fetoprotein (TUMOR MARKER) – most sensitive lab test for liver cancer (>200)
2. Liver BIOPSY — definitive method for diagnosis of metastatic liver cancer
Monitor prior to the procedure: Prothrombin time
BEFORE biopsy: position patient to LEFT side
AFTER biopsy: position patient to RIGHT side
Priority after: BLEEDING/ HEMORRHAGE
3. Chest CT SCAN and MRI— most accurate, to detect metastasis, lungs, brain, colon,
pancreas
4. Electrolyte study : hyponatremia, hypokalemia, and metabolic alkalosis.
5. Serum albumin and bilirubin levels: decreased; decrease serum levels of prothrombin
levels
Priority Nursing diagnosis: Acute pain related to abdominal pressure

Treatment: Radiation therapy (alone or with chemotherapy)
Medications
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1. Sorafenib (Nexavar) - is typically the first line treatment. is a kinase inhibitor; targeted
therapy that blocks kinase which plays roll in tumor growth (Decreased waist size
indicates improvement)
2. Cisplatin is a chemotherapy agent and is the second drug of choice for inoperable
liver cancer.
3. Systemic chemotherapy, such as doxorubicin, cisplatin, or fluorouracil
4. Analgesics: Morphine, fentanyl
5. Diuretics, spironolactone to reduce fluid overload. (Give Potassium chloride)
6. Lactulose (Cephulac) is administered to reduce serum ammonia levels. Two or three
soft stools per day are desirable; this indicates that lactulose is performing as intended.
( diet: moderate protein, fat, and carbohydrate diet.)
Treatment
1. Cryotherapy uses liquid nitrogen to FREEZE and destroy the tumor cells in the liver.
2. Radiation therapy uses ionizing radiation to KILL or control the tumor cells.
3. Radiofrequency ablation uses energy waves to heat and kill cancer cells.
4. Percutaneous ethanol injection, ethanol is directly injected into the tumor to kill the
cancerous cells.
5. Liver transplantation– offers the best chance of long-term survival for patients with
liver cancer.
 One lobe is resected from the donor
 donor liver is preserved in a solution and must be transplanted within 8 hours.
 Liver transplants are contraindicated for patients with cardiovascular disease
 Metronidazole is an antibiotic used for infection prophylaxis following
transplantation
 Cyclosporin is an immunosuppressant drug used to reduce the risk of organ
rejection.
 Cyclosporin, immunosuppressant, WOF: sore throat and fever (signs of Infection)
 Immunosuppressant drugs must be used for the rest of a patient's life after a liver
transplantation
 Acute graft rejection may occur from the 4th to 10th day after a liver
transplantation. The symptoms include tachycardia, pain in the right upper quadrant,
and change in bile color.
 Signs of acute graft rejection. fever, hypertension, graft tenderness, and malaise
Overview-Complications
Rupture — causing Peritonitis (WOF: hard, rigid or board like abdomen)
GI hemorrhage
Progressive cachexia
Liver failure and flzid overload
Hepatic, portal, or renal vein thrombosis
Nursing Considerations
L low-protein foods and high calorie diet
I Inspect dependent areas for edema; note the extent and degree of pitting, heart and lung
sound also
V verbalization of patient family feelings, concerns, and fears related to the condition is
encourages
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E encourage frequent turning and position changes, and use pressure-relief devices as
necessary.
R remember that drug METABOLISM is affected, take precaution in giving NSAIDS,
Adriamycin, and acetaminophens
PROSTATE CANCER
 2nd leading Cancer in men worldwide (2020)
 3rd leading cancer in men in Philippines (2015 to 2020)
 Prostate cancer is cancer that occurs in the prostate.
 The prostate is a small walnut-shaped gland in males
 below the bladder and in front of the rectum, surrounding the urethra
 highly treatable in the early stages
Most common: Adenocarcinoma

Location of most prostate cancers: peripheral zone, often posteriorly
ZONES of the prostate

1. peripheral - 65% of glandular tissue
2. central - 25% of gland
3. transitional - 10% of gland, where most BPH arises
RISK FACTOR:
A – age most important risk factor (Rare before age 40, common after 50, High after 65)
G – genetic · family history of more than one first-degree relative (father, son, or brother)
E – ethnicity: African-American race
Others: high intake of fat and red meat
WARNING SIGN: Changes in Bladder habit (decrease force of urine)

EARLY: Asymptomatic
LATE: Gross Hematuria
Most common clinical manifestation of prostate cancer in it's late stage is Gross hematuria
U urinary frequency, urgency, hesitancy, post-void dribbling
R retention of urine
I incontinence
N nocturia
E ejaculatory pain
S sensation of incomplete bladder emptying
Advanced metastasized prostate cancer
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B bone pain (backpain)

A anemia and weight loss
C cord compression and pathological fractures
K keep monitoring liver enzyme( elevated causing jaundice)
DIAGNOSTIC TEST
DRE- digital rectal exam. – Low cost, safe and ease of performance
PSA- prostate specific antigen
 Yearly PSA and DRE beginning at age 50.
 The normal range for a PSA test is 0-4 ng/mL.
 PSA level of 2.5-4 ng/ml requires further evaluation
 PSA over 10 is suspicious for cancer.
PSA Should be drawn BEFORE the DRE
 because the DRE can cause and increase in PSA due to prostatic irritation
BIOPSY — definitive test

Transrectal ultrasound (TRUS) is used to visualize the prostate for biopsy
Report after test: Difficulty urinating
MRI is used to determine Metastasis
Nursing Diagnosis: Impaired Urinary Elimination
Gleason score — for grading prostate cancer.
 Histologically graded on scale 1 (well diff) to 5 (poorly diff)

 TWO different specimens are taken and added
-2-4: slow growing, well diff
-5-7: intermediate
-8-10: aggressive, poorly diff
-higher: greater probability of extra capsular spread
ABCD STAGING
T1 (A) -T2 (B) - Confined to the prostate and was palpable during digital rectal examination
T3 (C )– The tumor has grown outside the prostate. It may have spread to the seminal
vesicle but NOT other organs.
T4 (D) – Palpable and has spread to other organs and often to distant sites such as bones or
lymph nodes
Medication:
1. Docetaxel - Preferred first line Chemotherapy in prostate cancer
- given with prednisone
2. Leuprolide (lupron) – GnRH agonist that suppresses luteinizing hormone
 decreases the production of testosterone
 Treatment for Advanced prostate cancer in males.
 Side effects of leuprolide. Bone loss and Hot Flashes
73
SURGERY: Radical prostatectomy (removal of entire prostate gland, prostatic capsule, and
seminal vesicles)
Others:
1. Transurethral needle ablation (TUNA) – uses low wave
radiofrequency to heat the prostate, causing necrosis destroys prostate tissue
2. Transurethral resection of the prostate (TURP) – the most common surgical
procedure to treat BPH and uses a RESECTOSCOPIC excision and cauterization of
prostate tissue.
 BLEEDING – IMMEDIATE DANGER should anticipate
 HEMORRHAGE is the most common complication of prostatectomy.
3. Perineal prostatectomy — may lead to SEXUAL DYSFUNCTIONS like impotence,
erectile dysfunction, and lack of libido
 increases the risk for infection because the incision is located close to the
anus and contamination with feces is possible.
CBI (continuous bladder irrigation) — for 3 days

PURPOSE OF CBI: to remove clots from the bladder and to prevent obstruction of the
catheter by clots.
C – catheter is draining thick, bright red clots and tissue: Increase the rate of the irrigation
L – Liquid/fluid intake increase up to 3L/day
O – observe /monitor for signs of urethral stricture: straining, dysuria
T – The amount of returned fluid (1,200 ml) should correspond to the amount of instilled fluid
S – Sequence of urine color
1st day after TURP: red urine or reddish pink
2nd day: pink urine
3rd – 4th day: clear urine.
MUST KNOWS:
1. Large amounts of blood or Frank bright bleeding should be reported.
2. Patients should EXPECT burning on urination and urinary frequency during the
first week.
3. Impotence or sexual dysfunction is NOT COMMON after TURP
4. Ambulate FIRST postop day if possible.
5. Continue adequate hydration
6. AVOID constipation and straining
7. AVOID strenuous activity, lifting, intercourse
8. AVOID engaging in sports for 3 to 4 weeks
9. DO NOT lift more than 10 pounds
10. Follow up appointments are important
LEUKEMIA
 a malignant increase in the number of ABNORMAL WBC (leukocytes) in
IMMATURE STAGE, in the BONE MARROW
CANCER SITE: BONE MARROW and lymphatic system
74
WBC — MAINLY affected blood cell

CAUSE: Idiopathic
LINK CAUSE: DNA mutation
Leukemia affects the bone marrow, causing: PANCYTOPENIA (LOW RBC, LOW WBC,
LOW PLATELETS)
L leukopenia —decreased WBC, increase infection from neutropenia

E erythropenia/anemia— decreased erythrocytes
T thrombocytopenia — decreased platelets, increase risk of bleeding
Risk factors
G Genetic disorders (DOWN SYNDROME) and FAMILY HISTORY

E Exposure to certain chemicals. (BENZENE)
N NO proven link between alcohol intake
E Exposure to high levels of radiation and previous cancer treatment
S Smoking cigarette most important ENVIRONMENTAL risk factor (lifestyle-related risk
factor)
SIGNS AND SYMPTOMS

HALLMARK: Fever and infection
L lymphadenopathy, hepatospleenomegaly and sore throat

E Easy bleeding (NOSEBLEED) or bruising and PETECHIAE
U unexplained weight loss
K key sign: fever and chills
E Excessive sweating, especially at night
M more and frequent infections
I increase weakness and persistent fatigue
A anemia (pallor)
CLASSIFICATION: IN TERMS OF PROGRESS

 Acute leukemia — Rapid and worsens quick, requires aggressive, timely
treatment.
 Chronic leukemia. — slow and can function normally for a period of time, can go
unnoticed or undiagnosed for years.
CLASSIFICATION: IN TERMS OF TYPES OF WBC AFFECTED

 Lymphocytic leukemia. — affects lymphoid cells (lymphocytes), which form
lymphoid or lymphatic tissue. Lymphatic tissue makes up your immune system.
 Myelogenous leukemia — affects the myeloid cells. Myeloid cells give rise to red
blood cells, white blood cells and platelet-producing cells.
75
The major types of leukemia are:

1. Acute lymphocytic leukemia (ALL). Abnormal leukocytes in blood-forming tissue. This
is the MOST COMMON type of leukemia in YOUNG CHILDREN. GOOD PROGNOSIS
2. Acute myelogenous leukemia (AML) — Inability of leukocytes to mature, MOST
COMMON type of acute leukemia in ADULTS. POOR PROGNOSIS
3. Chronic lymphocytic leukemia (CLL). With CLL, the most common chronic adult
leukemia, MOST patients are ASYMPTOMATIC
4. Chronic myelogenous leukemia (CML). Abnormal production of granulocytes
mainly affects oung to middle adults. A person with CML may have few or no symptoms
for months or years.
5. Hairy cell leukemia — Indolent leukemia of mature B-cells with infiltration of bone
marrow and spleen. Associated conditions autoimmune conditions. Characteristics
"hairy cells"
DIAGNOSIS
1. Physical exam
2. Blood tests.
3. Bone marrow test.
4. Bone marrow biopsy- confirmatory test for Leukemia large amount of immature
leukemic blast cells. Typing of protein markers to differentiate myeloid or lymphoid
Anesthesia: Local (lidocaine)
SITE OF BIOPSY:
Position of patient: Lateral Decubitus
Needle use: 21G and 23G
Posterior superior iliac crest- most common
Anterior superior iliac crest- for patients who can only lie supine
After a bone marrow biopsy : SUPINE for 2 hours
AFTER BIOPSY MONITOR: bleeding, and vital signs
# of NURSING ASSISTANT needed: 2
 Important to have 2 that 1 can prepare slides/specimen and the other can help
stabilize and position the patient
5. Bone marrow aspiration – Establishes diagnosis of ALL (Acute Lymphocytic leukemia)
Treatment
1. Chemotherapy. Chemotherapy is the major form of treatment for leukemia. This
drug treatment uses chemicals to kill leukemia cells.
 encourage the patient to purchase a wig or ,scarves or hat and wear it once
hair loss begins.
2. Targeted therapy. targeted drug treatments can cause cancer cells to die.
76
3. Radiation therapy. Uses X-rays or other high-energy beams to damage

leukemia cells and stop their growth.
4. Bone marrow transplant. stem cell transplant, helps reestablish healthy stem
cells by replacing unhealthy bone marrow with leukemia-free stem cells that will
regenerate healthy bone marrow.
5. Immunotherapy. Immunotherapy uses your immune system to fight cancer.
GENERAL CONSIDERATIONS
L LOW bacteria diet: avoid pepper, AVOID fresh fruits and fresh vegetables
E Ensure meticulous handwashing by all persons coming in contact with the client.
U Use soft bristle small tooth brush
K Keep patient in a PRIVATE ROOM, place patient in REVERSE ISOLATION
E ensure proper oral care , mucositis of mouth is common in clients receiving radiation to the
head and neck. (Use Saline or water)
M monitor weight 2x a week to monitor for weight loss
I Increase risk of infection and Injury are PRIORITY Nursing diagnosis
A Avoid flowers and plant. (Remove the fresh flowers from the client's room.)
1. Risk for infection — as a priority nursing diagnosis,

 notify the doctor if the child's temp exceeds 101 degrees F
 Ambulate inside room NOT hallways
 AVOID CROWDS
 AVOID exposure to person with colds
 increase the use of humidifiers throughout then house
2. A potential for injury

 Low platelet increases risk of bleeding from even minor injuries.
 Safety measures: shave with an electric razor, use soft tooth brush, avoid SQ or IM
meds and invasive procedures (urinary drainage catheter or a nasogastric tube)
 Side-rails up, remove sharp objects, frequently assess for signs of bleeding, bruising,
hemorrhage.
LIVER CANCER
 Malignant cells growing in the tissues of the liver
 Rapidly fatal, usually within 6 months if unresectable
 Second leading cause of fatal hepatic disease (after cirrhosis)
 The liver is one of the most common sites of metastasis from other primary cancers.
 Most primary liver tumors (90%) are hepatomas originating in the parenchymal cells.
 Survival year is 5 YEARS
3. Primary liver cancer – hepatocellular cancer

 more common in MEN with chronic liver disease.
77
 More common in developed countries

4. Secondary liver cancer – secondary liver cancer is much more common than primary
liver cancer
 metastatic liver cancer (colorectal, breast and lung)
Incidence: Men, more that 55 years old
Most common risk factor: HBV and HCV infection

3. America– hepatitis C
4. Asia – hepatitis B
Risk Factors
L liver cirrhosis
I intake of alcohol, foods with AFLATOXIN, RED MEATS and saturated fats
V viral infection (chronic Hepa B and C)
E extra fat in the liver not caused by alcohol (non alcoholic fatty liver disease
R race: Asian and Pacific Islanders (highest rates of liver cancer), Black American
Others: DM, OBESITY, Wilson's disease, Autoimmune liver disease, Hemochromatosis
SIGNS/SYMPTOMS:
Warning sign: Epigastric or RUQ pain and unexplained weight loss
Early signs
Splenomegaly
Hepatomegaly
Ascites (increase abdominal girth)
Fatigue
Peripheral edema
Portal hypertension
Late signs
Anorexia
Weight loss and cachexia
Fever/chills
Jaundice
Palpable mass
Right upper quadrant tenderness dull abdominal pain in epigastric
DIAGNOSTIC TEST
6. Alpha fetoprotein (TUMOR MARKER) – most sensitive lab test for liver cancer (>200)
7. Liver BIOPSY — definitive method for diagnosis of metastatic liver cancer
Monitor prior to the procedure: Prothrombin time
BEFORE biopsy: position patient to LEFT side
AFTER biopsy: position patient to RIGHT side
Priority after: BLEEDING/ HEMORRHAGE
78
8. Chest CT SCAN and MRI— most accurate, to detect metastasis, lungs, brain, colon,
pancreas
9. Electrolyte study : hyponatremia, hypokalemia, and metabolic alkalosis.
10. Serum albumin and bilirubin levels: decreased; decrease serum levels of prothrombin
levels
Priority Nursing diagnosis: Acute pain related to abdominal pressure
Treatment: Radiation therapy (alone or with chemotherapy)
Medications
7. Sorafenib (Nexavar) - is typically the first line treatment. is a kinase inhibitor; targeted
therapy that blocks kinase which plays roll in tumor growth (Decreased waist size
indicates improvement)
8. Cisplatin is a chemotherapy agent and is the second drug of choice for inoperable
liver cancer.
9. Systemic chemotherapy, such as doxorubicin, cisplatin, or fluorouracil
10. Analgesics: Morphine, fentanyl
11. Diuretics, spironolactone to reduce fluid overload. (Give Potassium chloride)
12. Lactulose (Cephulac) is administered to reduce serum ammonia levels. Two or three
soft stools per day are desirable; this indicates that lactulose is performing as intended.
( diet: moderate protein, fat, and carbohydrate diet.)
Treatment
6. Cryotherapy uses liquid nitrogen to FREEZE and destroy the tumor cells in the liver.
7. Radiation therapy uses ionizing radiation to KILL or control the tumor cells.
8. Radiofrequency ablation uses energy waves to heat and kill cancer cells.
9. Percutaneous ethanol injection, ethanol is directly injected into the tumor to kill the
cancerous cells.
10. Liver transplantation– offers the best chance of long-term survival for patients with
liver cancer.
 One lobe is resected from the donor
 donor liver is preserved in a solution and must be transplanted within 8 hours.
 Liver transplants are contraindicated for patients with cardiovascular disease
 Metronidazole is an antibiotic used for infection prophylaxis following
transplantation
 Cyclosporin is an immunosuppressant drug used to reduce the risk of organ
rejection.
 Cyclosporin, immunosuppressant, WOF: sore throat and fever (signs of Infection)
 Immunosuppressant drugs must be used for the rest of a patient's life after a liver
transplantation
 Acute graft rejection may occur from the 4th to 10th day after a liver
transplantation. The symptoms include tachycardia, pain in the right upper quadrant,
and change in bile color.
 Signs of acute graft rejection. fever, hypertension, graft tenderness, and malaise
Overview-Complications
Rupture — causing Peritonitis (WOF: hard, rigid or board like abdomen)
GI hemorrhage
Progressive cachexia
79
Liver failure and flzid overload

Hepatic, portal, or renal vein thrombosis
Nursing Considerations
L low-protein foods and high calorie diet
I Inspect dependent areas for edema; note the extent and degree of pitting, heart and lung
sound also
V verbalization of patient family feelings, concerns, and fears related to the condition is
encourages
E encourage frequent turning and position changes, and use pressure-relief devices as
necessary.
R remember that drug METABOLISM is affected, take precaution in giving NSAIDS,
Adriamycin, and acetaminophens
PROSTATE CANCER
 2nd leading Cancer in men worldwide (2020)
 3rd leading cancer in men in Philippines (2015 to 2020)
 Prostate cancer is cancer that occurs in the prostate.
 The prostate is a small walnut-shaped gland in males
 below the bladder and in front of the rectum, surrounding the urethra
 highly treatable in the early stages
Most common: Adenocarcinoma

Location of most prostate cancers: peripheral zone, often posteriorly
ZONES of the prostate

4. peripheral - 65% of glandular tissue
5. central - 25% of gland
6. transitional - 10% of gland, where most BPH arises
RISK FACTOR:
A – age most important risk factor (Rare before age 40, common after 50, High after 65)
G – genetic · family history of more than one first-degree relative (father, son, or brother)
E – ethnicity: African-American race
Others: high intake of fat and red meat
WARNING SIGN: Changes in Bladder habit (decrease force of urine)

EARLY: Asymptomatic
LATE: Gross Hematuria
Most common clinical manifestation of prostate cancer in it's late stage is Gross hematuria
U urinary frequency, urgency, hesitancy, post-void dribbling
R retention of urine
80
I incontinence
N nocturia
E ejaculatory pain
S sensation of incomplete bladder emptying
Advanced metastasized prostate cancer

B bone pain (backpain)
A anemia and weight loss
C cord compression and pathological fractures
K keep monitoring liver enzyme( elevated causing jaundice)
DIAGNOSTIC TEST
DRE- digital rectal exam. – Low cost, safe and ease of performance
PSA- prostate specific antigen
 Yearly PSA and DRE beginning at age 50.
 The normal range for a PSA test is 0-4 ng/mL.
 PSA level of 2.5-4 ng/ml requires further evaluation
 PSA over 10 is suspicious for cancer.
PSA Should be drawn BEFORE the DRE
 because the DRE can cause and increase in PSA due to prostatic irritation
BIOPSY — definitive test

Transrectal ultrasound (TRUS) is used to visualize the prostate for biopsy
Report after test: Difficulty urinating
MRI is used to determine Metastasis
Nursing Diagnosis: Impaired Urinary Elimination
Gleason score — for grading prostate cancer.
 Histologically graded on scale 1 (well diff) to 5 (poorly diff)

 TWO different specimens are taken and added
-2-4: slow growing, well diff
-5-7: intermediate
-8-10: aggressive, poorly diff
-higher: greater probability of extra capsular spread
ABCD STAGING
T1 (A) -T2 (B) - Confined to the prostate and was palpable during digital rectal examination
T3 (C )– The tumor has grown outside the prostate. It may have spread to the seminal
vesicle but NOT other organs.
T4 (D) – Palpable and has spread to other organs and often to distant sites such as bones or
lymph nodes
Medication:
81
3. Docetaxel - Preferred first line Chemotherapy in prostate cancer

- given with prednisone
4. Leuprolide (lupron) – GnRH agonist that suppresses luteinizing hormone
 decreases the production of testosterone
 Treatment for Advanced prostate cancer in males.
 Side effects of leuprolide. Bone loss and Hot Flashes
SURGERY: Radical prostatectomy (removal of entire prostate gland, prostatic capsule, and
seminal vesicles)
Others:
4. Transurethral needle ablation (TUNA) – uses low wave
radiofrequency to heat the prostate, causing necrosis destroys prostate tissue
5. Transurethral resection of the prostate (TURP) – the most common surgical
procedure to treat BPH and uses a RESECTOSCOPIC excision and cauterization of
prostate tissue.
 BLEEDING – IMMEDIATE DANGER should anticipate
 HEMORRHAGE is the most common complication of prostatectomy.
6. Perineal prostatectomy — may lead to SEXUAL DYSFUNCTIONS like impotence,
erectile dysfunction, and lack of libido
 increases the risk for infection because the incision is located close to the
anus and contamination with feces is possible.
CBI (continuous bladder irrigation) — for 3 days

PURPOSE OF CBI: to remove clots from the bladder and to prevent obstruction of the
catheter by clots.
C – catheter is draining thick, bright red clots and tissue: Increase the rate of the irrigation
L – Liquid/fluid intake increase up to 3L/day
O – observe /monitor for signs of urethral stricture: straining, dysuria
T – The amount of returned fluid (1,200 ml) should correspond to the amount of instilled fluid
S – Sequence of urine color
1st day after TURP: red urine or reddish pink
2nd day: pink urine
3rd – 4th day: clear urine.
MUST KNOWS:
1. Large amounts of blood or Frank bright bleeding should be reported.
2. Patients should EXPECT burning on urination and urinary frequency during the
first week.
3. Impotence or sexual dysfunction is NOT COMMON after TURP
4. Ambulate FIRST postop day if possible.
5. Continue adequate hydration
6. AVOID constipation and straining
7. AVOID strenuous activity, lifting, intercourse
8. AVOID engaging in sports for 3 to 4 weeks
9. DO NOT lift more than 10 pounds
82
10. Follow up appointments are important
LEUKEMIA
 a malignant increase in the number of ABNORMAL WBC (leukocytes) in
IMMATURE STAGE, in the BONE MARROW
CANCER SITE: BONE MARROW and lymphatic system

WBC — MAINLY affected blood cell
CAUSE: Idiopathic
LINK CAUSE: DNA mutation
Leukemia affects the bone marrow, causing: PANCYTOPENIA (LOW RBC, LOW WBC,
LOW PLATELETS)
L leukopenia —decreased WBC, increase infection from neutropenia

E erythropenia/anemia— decreased erythrocytes
T thrombocytopenia — decreased platelets, increase risk of bleeding
Risk factors
G Genetic disorders (DOWN SYNDROME) and FAMILY HISTORY

E Exposure to certain chemicals. (BENZENE)
N NO proven link between alcohol intake
E Exposure to high levels of radiation and previous cancer treatment
S Smoking cigarette most important ENVIRONMENTAL risk factor (lifestyle-related risk
factor)
SIGNS AND SYMPTOMS

HALLMARK: Fever and infection
L lymphadenopathy, hepatospleenomegaly and sore throat

E Easy bleeding (NOSEBLEED) or bruising and PETECHIAE
U unexplained weight loss
K key sign: fever and chills
E Excessive sweating, especially at night
M more and frequent infections
I increase weakness and persistent fatigue
A anemia (pallor)
CLASSIFICATION: IN TERMS OF PROGRESS

 Acute leukemia — Rapid and worsens quick, requires aggressive, timely
treatment.
 Chronic leukemia. — slow and can function normally for a period of time, can go
unnoticed or undiagnosed for years.
CLASSIFICATION: IN TERMS OF TYPES OF WBC AFFECTED
83
 Lymphocytic leukemia. — affects lymphoid cells (lymphocytes), which form

lymphoid or lymphatic tissue. Lymphatic tissue makes up your immune system.
 Myelogenous leukemia — affects the myeloid cells. Myeloid cells give rise to red
blood cells, white blood cells and platelet-producing cells.
The major types of leukemia are:

6. Acute lymphocytic leukemia (ALL). Abnormal leukocytes in blood-forming tissue. This
is the MOST COMMON type of leukemia in YOUNG CHILDREN. GOOD PROGNOSIS
7. Acute myelogenous leukemia (AML) — Inability of leukocytes to mature, MOST
COMMON type of acute leukemia in ADULTS. POOR PROGNOSIS
8. Chronic lymphocytic leukemia (CLL). With CLL, the most common chronic adult
leukemia, MOST patients are ASYMPTOMATIC
9. Chronic myelogenous leukemia (CML). Abnormal production of granulocytes
mainly affects oung to middle adults. A person with CML may have few or no symptoms
for months or years.
10. Hairy cell leukemia — Indolent leukemia of mature B-cells with infiltration of bone
marrow and spleen. Associated conditions autoimmune conditions. Characteristics
"hairy cells"
DIAGNOSIS
6. Physical exam
7. Blood tests.
8. Bone marrow test.
9. Bone marrow biopsy- confirmatory test for Leukemia large amount of immature
leukemic blast cells. Typing of protein markers to differentiate myeloid or lymphoid
Anesthesia: Local (lidocaine)
SITE OF BIOPSY:
Position of patient: Lateral Decubitus
Needle use: 21G and 23G
Posterior superior iliac crest- most common
Anterior superior iliac crest- for patients who can only lie supine
After a bone marrow biopsy : SUPINE for 2 hours
AFTER BIOPSY MONITOR: bleeding, and vital signs
# of NURSING ASSISTANT needed: 2
 Important to have 2 that 1 can prepare slides/specimen and the other can help
stabilize and position the patient
10. Bone marrow aspiration – Establishes diagnosis of ALL (Acute Lymphocytic leukemia)
84
Treatment
1. Chemotherapy. Chemotherapy is the major form of treatment for leukemia. This
drug treatment uses chemicals to kill leukemia cells.
 encourage the patient to purchase a wig or ,scarves or hat and wear it once
hair loss begins.
2. Targeted therapy. targeted drug treatments can cause cancer cells to die.
3. Radiation therapy. Uses X-rays or other high-energy beams to damage
leukemia cells and stop their growth.
4. Bone marrow transplant. stem cell transplant, helps reestablish healthy stem
cells by replacing unhealthy bone marrow with leukemia-free stem cells that will
regenerate healthy bone marrow.
5. Immunotherapy. Immunotherapy uses your immune system to fight cancer.
GENERAL CONSIDERATIONS
L LOW bacteria diet: avoid pepper, AVOID fresh fruits and fresh vegetables
E Ensure meticulous handwashing by all persons coming in contact with the client.
U Use soft bristle small tooth brush
K Keep patient in a PRIVATE ROOM, place patient in REVERSE ISOLATION
E ensure proper oral care , mucositis of mouth is common in clients receiving radiation to the
head and neck. (Use Saline or water)
M monitor weight 2x a week to monitor for weight loss
I Increase risk of infection and Injury are PRIORITY Nursing diagnosis
A Avoid flowers and plant. (Remove the fresh flowers from the client's room.)
3. Risk for infection — as a priority nursing diagnosis,

 notify the doctor if the child's temp exceeds 101 degrees F
 Ambulate inside room NOT hallways
 AVOID CROWDS
 AVOID exposure to person with colds
 increase the use of humidifiers throughout then house
4. A potential for injury

 Low platelet increases risk of bleeding from even minor injuries.
 Safety measures: shave with an electric razor, use soft tooth brush, avoid SQ or IM
meds and invasive procedures (urinary drainage catheter or a nasogastric tube)
 Side-rails up, remove sharp objects, frequently assess for signs of bleeding, bruising,
hemorrhage.
85
86
87

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COPYRIGHT: JONAS MARVIN M.

MEDICAL SURGICAL NURSING | ENDOCRINE DISORDERS

The hypothalamus and pituitary gland are neuroendocrine organs.

Endocrine Versus Exocrine gland

hormone is an "intercellular signal" — chemical substance, a molecule that is secreted by one

Pituitary gland— a pea-sized gland, known as the MASTER GLAND

S/sx onset: 20-40 years old

Signs and symptoms:

J – joint paint (arthritis) , weakness and severe headache

Best time to buy shoes: late afternoon/evening.

2. Growth hormone suppression test.– best method to confirm acromegaly.

Treatment: combination of surgery, radiation, and drug therapy

After surgery: Assessment of AIRWAY is priority.

Drug of choice: Parlodel

 Avoid somatropin (Genotropin) drug

Complications: Cardiomegaly, Heart failure, DM, HTN

2. Gigantism — condition brought about by overproduction of growth hormone by the

Cause: adenoma, a tumor of the pituitary gland.

Symptom of gigantism is characterized by: Weakness

SIGNS AND SYMPTOMS

G – gaps between teeth, prominent forehead and jaw

3. GALACTORRHEA production of breast milk in men or in women who are NOT

CAUSE: Pituitary tumor (prolactinoma)– overproduction of the hormone prolactin

Hallmark: unexpected breast milk production

Signs and Symptoms

COLLABORATIVE approach: Endocrinologist and Ophthalmologist for visual problems

TAKE NOTE: TSH is NOT produce by thyroid gland

EUTHYROIDISM — Normal functioning of thyroid gland

Three types of thyroid disorders:

1. Hyperthyroidism – Hyperthyroidism is the overactivity of the thyroid gland

Primary disease: Grave's disease (most common cause)

Hyperthyroidism risk factors

Graves disease (hyperthyroidism with toxic goiter)

HYPERTHYROIDISM Hallmark Sign: Poor Thermoregulation and Heat intolerance

HYPERTHYROIDISM Signs and Symptoms:

Personality changes: moody, manic, Emotional lability, decrease attention span

Hyperthyroidism Nursing Diagnosis:

HIGHEST PRIORITY NURSING DIAGNOSIS: Imbalanced nutrition: LESS than body

Hyperthyroidism Diagnostic tests

Hyperthyroid labs: decreased TSH, increased T3 and T4

Drug of Choice: Propylthiouracil-PTU

Adverse side effects are:

Y – you may loss taste

Others: methimazole 15-60mg/day PO – fewer side effects, treatment of graves disease, do

Radioactive Iodine Therapy

Safety Precautions for the Patient Receiving an Unsealed Radioactive Isotope

PreOp drug: Saturated solution of potassium iodide (SSKI)

Postop care of subtotal thyroidectomy

IMPORTANT INTERVENTIONS: coughing (deep breathing), splinting wound, respiratory

POST OP POSITION: SEMI FOWLERS

 have suction, oxygen, and a tracheostomy set available within 24 hours

3. laryngeal nerve damage

WOF: Thyroid storm or thyrotoxicosis

Thyroid storm manifestations

Nursing interventions for thyroid storm

3. Iodide solution: blocks SECRETION of TH (like Lugol's solution=taste changes

Hypothyroid Risks factors

T – Thick, brittle nails, Thick, dry scaly skin, Thick tongue

Hypothyroidism Diagnostic Tests