o hemorrhage, perforation, pyloric obstruction, and
PEPTIC ULCER DISEASE
· Gastric Ulcers
➔ Usually develop in the antrum of the stomach
➔ Results from Acid-back diffusion or
dysfunction of the pyloric sphincter
➔ Delayed gastric emptying = causes
regurgitation of duodenal contents, which
worsens the gastric mucosal injury
➔ Gastric ulcers are deep and penetrating, and
they usually occur on the lesser curvature of
the stomach, near the pylorus
· Duodenal Ulcers
➔ Upper portion of the duodenum
➔ deep, sharply demarcated lesions that
penetrate through the mucosa and submucosa
into the muscularis propria
➔ The main feature of a duodenal ulcer is high
gastric acid secretion
➔ Combined with hypersecretion, a rapid
emptying of food from the stomach reduces
the buffering effect of food and delivers a large
acid bolus to the duodenum
· Stress Ulcers
➔ Bleeding caused by gastric erosion is the main
manifestation of acute stress ulcers.
➔ extensive burns (Curling's ulcer)
➔ sepsis (ischemic ulcer)
➔ increased intracranial pressure (Cushing's
ulcer)
COMPLICATIONS OF PUD
o Peptic ulcer disease is caused most often by
intractable disease
o Hemorrhage is the most serious complication. It
tends to occur more often in patients with gastric
ulcers and in older adults.
o Melena may occur in patients with gastric ulcers but
is more common in those with duodenal ulcers.
o Gastric acid digestion of blood typically results in a
granular dark vomitus (coffee-ground appearance).
o Peritonitis = The abdomen is tender, rigid, and
boardlike, patient often assumes a “fetal” position to
decrease the tension on the abdominal muscles,
Peristalsis diminishes, and paralytic ileus develops
o Pyloric obstruction = occurs in a small
percentage of patients and is manifested by vomiting
caused by stasis and gastric dilation
o Symptoms of obstruction include abdominal
bloating, nausea, and vomiting
o When vomiting persists, the patient may have
hypochloremic (metabolic) alkalosis from loss of large
quantities of acid gastric juice (hydrogen and chloride
ions) in the vomitus. Hypokalemia may also result
from the vomiting or metabolic alkalosis.
ETIOLOGY OF PUD
bacterial infection with H. pylori and NSAIDs
o corticosteroids (e.g., prednisone), theophylline
(Theo-Dur), and caffeine stimulate hydrochloric acid
production. Patients receiving radiation therapy may
also develop GI ulcers
NURSING RESPONSIBILITIES
o Review all prescription and OTC drugs the patient
is taking. Specifically inquire whether the patient is
taking corticosteroids, chemotherapy, or NSAIDs.
o Inquire about any changes in the character of the
pain. For example, if pain that was once intermittent
and relieved by food and antacids becomes constant
and radiates to the back or upper quadrant, the
patient may have ulcer perforation
o PA FINDINGS
➔ epigastric tenderness, located at the midline
between the umbilicus and the xiphoid
process
➔ Perforation = rigid, boardlike abdomen
accompanied by rebound tenderness and
pain.
➔ Dyspepsia (indigestion) is the most commonly
reported symptom associated with PUD =
described as sharp, burning, or gnawing pain.
➔ Gastric ulcer pain = upper epigastrium with
localization to the left of the midline and is
aggravated by food
➔ Duodenal ulcer pain = right of or below the
epigastrium. The pain associated with a
duodenal ulcer occurs 90 minutes to 3 hours
 after eating and often awakens the patient at
night
➔ To assess for fluid volume deficit that occurs
from bleeding, take orthostatic blood
pressures and monitor for signs and
symptoms of dehydration. Also assess for
dizziness, especially when the patient is
upright, because this is a symptom of fluid
volume deficit.
DIAGNOSTIC ASSESSMENT FOR PUD
➔ The major diagnostic test for PUD is
esophagogastroduodenoscopy (EGD), which
is the most accurate means of establishing a
diagnosis.
➔ EGD may be repeated at 4- to 6-week
intervals while the health care provider
evaluates the progress of healing in response
to therapy
MEDICAL MANAGEMENT
➔ Proton pump inhibitors (PPIs) is the drug
class of choice for treating patients with acid-
related disorders. (ZOLE)
- PPIs should not be discontinued abruptly to
prevent rebound activation of the proton pump.
Therefore, a step-down approach over several days is
recommended
➔ H2 -receptor antagonists block the action of
the H2 receptors of the parietal cells, thus
inhibiting gastric acid secretion (TIDINE)
- These drugs are typically administered in a
single dose at bedtime and are used for 4 to 6 weeks
in combination with other therapy
➔ Antacids buffer gastric acid and prevent the
formation of pepsin. They may help small
duodenal ulcers heal but are usually not used
alone as drug therapy
- Mylanta and Maalox are examples: These
products must be administered cautiously to patients
with renal impairment because elimination is reduced
and excessive amounts are retained in the body
· For optimal effect, take antacids about 2
hours after meals to reduce the hydrogen ion load
in the duodenum. Antacids may be effective from
30 minutes to 3 hours after ingestion. If taken on
an empty stomach, they 3239 are quickly
evacuated. Thus the neutralizing effect is reduced
- Calcium carbonate (Tums) is a potent antacid,
but it triggers gastrin release, causing a rebound acid
secretion. Therefore its use in acid inhibition is not
recommended.
➔ Sucralfate (Carafate) is a mucosal barrier
fortifier (protector) that forms complexes with
proteins at the base of a peptic ulcer. This
protective coat prevents further digestive
action of both acid and pepsin
- Sucralfate is given on an empty stomach 1 hour
before each meal and at bedtime. The main side
effect of this drug is constipation.
➔ Bismuth subsalicylate (Pepto-Bismol)
inhibits H. pylori from binding to the mucosal
lining and stimulates mucosal protection and
prostaglandin production
- Patients should also be taught that this
medication may cause the stools to be discolored
black. This discoloration is temporary and harmless.
NONSURGICAL MANAGEMENT OF PUD
· Upper GI Bleeding
- Fluid Replacement: Volume replacement
with isotonic solutions (e.g., 0.9% normal saline
solution, lactated Ringer's solution) should be
started immediately. The health care provider
may prescribe blood products such as packed
red blood cells to expand volume and correct a
low hemoglobin and hematocrit
- Nasogastric Tube placement and Lavage:
insert a large-bore nasogastric tube (NGT) to
➔ Determine the presence or absence of blood
in the stomach
➔ gastric lavage requires the insertion of a large-
bore NGT with instillation of a room-
temperature solution in volumes of 200 to 300
mL. The solution and blood are repeatedly
withdrawn manually until returns are clear or
light pink and without clots.
ENDOSCOPIC THERAPY Nx. Responsibilities
➔ Pre-EGD nursing care involves inserting one
or two large-bore IV catheters if they are not in
place. A large catheter allows the patient to
 receive IV moderate sedation and possibly a
blood transfusion
➔ Keep the patient NPO for 4 to 6 hours before
the procedure. This prevents the risk for
aspiration and allows the endoscopist to view
and treat the ulcer.
➔ A patient must sign a consent form before the
EGD after the physician informs him or her
about the procedure.
➔ After EGD, monitor vital signs, heart rhythm,
and oxygen saturation frequently until they
return to baseline.
➔ In addition, frequently assess the patient's
ability to swallow saliva. The patient's gag
reflex may initially be absent after an EGD
because of anesthetizing (numbing) the throat
with a spray before the procedure. After the
procedure, do not allow the patient to have
food or liquids until the gag reflex is intact
HYPERPARATHYROIDISM
· The parathyroid glands maintain calcium and
phosphate balance
· Increased levels of parathyroid hormone
(PTH) act directly on the kidney, causing
increased kidney reabsorption of calcium and
increased phosphorus excretion
· In hyperparathyroidism, these processes
cause hypercalcemia (excessive calcium) and
hypophosphatemia (inadequate blood phosphorus
level).
· Excess PTH = increase bone resorption
(bone loss of calcium) by decreasing osteoblastic
(bone production) activity and increasing
osteoclastic (bone destruction) activity =>
releases calcium and phosphorus into the blood
and reduces bone density. With chronic calcium
excess and hypercalcemia, calcium is deposited
in soft tissues.
ASSESSMENT
➔ bone fractures, recent weight loss, arthritis, or
psychological stress
➔ Ask whether the patient has received radiation
treatment to the head or neck.
➔ Chronic hyperparathyroidism = waxy pallor of
the skin and bone deformities in the
extremities and back.
➔ High levels of PTH cause kidney stones and
deposits of calcium in the soft tissue of the
kidney
➔ GI problems (e.g., anorexia, nausea, vomiting,
epigastric pain, constipation, weight loss) are
common when serum calcium levels are high.
➔ Elevated serum gastrin levels are caused by
hypercalcemia and lead to peptic ulcer
disease.
➔ When serum calcium levels are greater than
12 mg/dL, the patient may have psychosis
with mental confusion, which leads to coma
and death if left untreated.
NONSURGICAL MANAGEMENT:
HYPERPARATHYROIDISM
➔ Diuretic and hydration therapies are used
for reducing serum calcium levels in patients
who have milder disease = Usually
furosemide (Lasix, Uritol ), a diuretic that
increases kidney excretion of calcium, is used
together with IV saline in large volumes to
promote calcium excretion
➔ For severe manifestations = cinacalcet
(Sensipar). When taken orally, the drug binds
to calcium-sensitive receptors on parathyroid
tissue. This binding reduces PTH production
and release.
➔ Monitor cardiac function and intake and
output every 2 hours during hydration therapy
➔ Preventing injury is important because the
patient with chronic hyperparathyroidism often
has significant bone density loss and is at risk
for pathologic fractures
SURGICAL MANAGEMENT:
HYPERPARATHYROIDISM
Parathyroidectomy
- Before surgery the patient is stabilized and
calcium levels are decreased to near normal.
- Nursing care before and after surgical removal of
the parathyroid glands is the same as that for
thyroidectomy
➔ A hypocalcemic crisis can occur post-
surgically
- Monitor for manifestations of hypocalcemia, such
as tingling and twitching in the extremities and face.
Check for Trousseau's and Chvostek's signs, either of
which indicates potential tetany
- The recurrent laryngeal nerve can be
damaged. Assess the patient for changes in voice
patterns and hoarseness.
HYPOPARATHYROIDISM
· Whether the problem is a lack of PTH
secretion or an ineffectiveness of PTH on tissues,
the result is the same: hypocalcemia
· Hypomagnesemia (decreased serum
magnesium levels) may also cause
hypoparathyroidism. It causes impairment of PTH
secretion and may interfere with the effects of
PTH on the bones, kidneys, and calcium
regulation.
ASSESSMENT
➔ Ask about any head or neck surgery or
radiation therapy because these treatments
may damage the parathyroid glands and
cause hypoparathyroidism
➔ Tingling and numbness around the mouth or in
the hands and feet reflect mild to moderate
hypocalcemia
➔ Severe muscle cramps, spasms of the hands
and feet, and seizures (with no loss of
consciousness or incontinence) reflect 3714 a
more severe hypocalcemia
➔ Bands or pits may encircle the crowns of the
teeth, which indicate a loss of calcium from the
teeth with enamel loss
➔ Serum calcium, phosphorus, magnesium,
vitamin D, and urine cyclic adenosine
monophosphate (cAMP) levels may be used in
the diagnostic workup for hypoparathyroidism
(see Chart 63-10). The CT scan can show
brain calcifications, which indicate chronic
hypocalcemia.
HYPERTHYROIDISM
● Thyroid hormones increase metabolism in all
body organs
● The excessive thyroid hormones stimulate most
body systems, causing hypermetabolism and
increased sympathetic nervous system activity.
● Thyroid hormones stimulate the heart, increasing
both heart rate and stroke volume. These
responses increase cardiac output, systolic blood
pressure, and blood flow
● Elevated thyroid hormone levels affect protein,
fat, and glucose metabolism. Protein buildup and
breakdown are increased, but breakdown
exceeds buildup, causing a net loss of body
protein known as a negative nitrogen balance
● Glucose tolerance is decreased, and the patient
has hyperglycemia
● Fat metabolism is increased, and body fat
decreases. Although the patient has an
increased appetite, the increased metabolism
causes weight loss and nutrition deficits.
● Thyroid hormones are produced in response to
the stimulation hormones secreted by the
hypothalamus and anterior pituitary glands
Grave’s Disease
● Also called toxic diffuse goiter
● Graves' disease is an autoimmune disorder
resulting from Hashimoto's thyroiditis
● In Graves' disease, all the general manifestations
of hyperthyroidism are present.
● In addition, other manifestations specific to
Graves' disease may occur, including
exophthalmos (abnormal protrusion of the eyes)
and pretibial myxedema (dry, waxy swelling of
the front surfaces of the lower legs that
resembles benign tumors or keloids). Not all
patients with a goiter have hyperthyroidism.
● Graves' disease can occur at any age but is
diagnosed most often in women between 20 and
40 years of age
● Toxic multinodular goiter usually occurs after the
age of 50 years and affects women 4 times more
often than men
ASSESSMENT
➔ A hallmark of hyperthyroidism is poor
thermoregulation with heat intolerance
➔ The patient may also report palpitations or chest
pain as a result of the cardiovascular effects. Ask
about changes in breathing patterns, because
dyspnea (with or without exertion) is common
➔ Visual changes may be the earliest problem the
patient or family notices, especially exophthalmos
with Graves' disease
➔ Fatigue and insomnia are common.
➔ Initially, both men and women may have an
increase in libido, but this changes as the patient
becomes more fatigued.
➔ Amenorrhea in women
CLINICAL MANIFESTATIONS: HYPERTHYROIDISM
➔ Exophthalmos: The wide-eyed or “startled” look
is due to edema in the extraocular muscles and
increased fatty tissue behind the eye, which
pushes the eyeball forward and may cause
problems with focusing
➔ Pressure on the optic nerve may impair vision
➔ Observe the eyes for excessive tearing and a
bloodshot appearance. (+) Photosensitivity
➔ Two other eye problems are common in all types
of hyperthyroidism: eyelid retraction (eyelid lag)
and globe (eyeball) lag
➔ Bruits (turbulence from increased blood flow) may
be heard in the neck with a stethoscope
➔ Inspect the hair and skin. Fine, soft, silky hair
and smooth, warm, moist skin are common
➔ Many patients notice thinning of scalp hair.
DIAGNOSTIC ASSESSMENT
➔ Thyroid scan evaluates the position, size, and
functioning of the thyroid gland
➔ Radioactive iodine (RAI [ 123 I]) is given by
mouth, and the uptake of iodine by the thyroid
gland (radioactive iodine uptake [RAIU]) is
measured.
➔ Ultrasonography of the thyroid gland can
determine its size and the general composition of
any masses or nodules. This procedure takes
about 30 minutes to perform and is painless.
➔ Electrocardiography (ECG) usually shows
tachycardia. Other ECG changes with
hyperthyroidism include atrial fibrillation,
dysrhythmias, and changes in P and T
waveforms.
SURGICAL MANAGEMENT
➔ Removal of all (total thyroidectomy) or part
(subtotal thyroidectomy) of the thyroid tissue
decreases the production of thyroid hormones.
After a total thyroidectomy, patients must take
lifelong thyroid hormone replacement.
➔ PREOP CARE: The patient is treated with
thionamide drug therapy first to have near-normal
thyroid function (euthyroid) before thyroid
surgery.
➔ Iodine preparations also are used to decrease
thyroid size and vascularity, thereby reducing the
risk for hemorrhage and the potential for thyroid
storm during surgery
➔ Hypertension, dysrhythmias, and tachycardia
must be controlled before surgery.
➔ Teach the patient to perform deep-breathing
exercises. Stress the importance of supporting
the neck when coughing or moving by placing
both hands behind the neck to reduce strain on
the incision.
➔ Explain that hoarseness may be present for a
few days as a result of endotracheal tube
placement during surgery.
➔ OPERATIVE CARE: the parathyroid glands and
recurrent laryngeal nerves are avoided to reduce
the risk for complications and injury. Usually,
general anesthesia is used even for the minimally
invasive techniques
➔ POSTOP CARE: Monitor vital signs every 15
minutes until the patient is stable and then every
30 minutes
➔ Use pillows to support the head and neck. Place
the patient, while he or she is awake, in a
semiFowler's position
➔ Assist the patient to deep-breathe every 30
minutes to 1 hour. Suction oral and tracheal
secretions when necessary
➔ Thyroid surgery can cause: hemorrhage,
respiratory distress, parathyroid gland injury,
damage to the laryngeal nerves, and thyroid storm
➔ POSTOP: Thyroidectomy cont.
➔ Hemorrhage is most likely to occur during the first
24 hours after surgery. Inspect the neck dressing
and behind the patient's neck for blood
➔ Respiratory distress can result from swelling,
tetany, or damage to the laryngeal nerve resulting
in spasms. Laryngeal stridor (harsh, highpitched
respiratory sounds) is heard in acute respiratory
obstruction
➔ Hypocalcemia and tetany may occur if the
parathyroid glands are removed or damaged or
their blood supply is impaired during thyroid
surgery, resulting in decreased parathyroid
hormone (PTH) levels.
➔ Ask the patient hourly about tingling around the
mouth or of the toes and fingers
➔ Calcium gluconate or calcium chloride for IV use
should be available in an emergency situation.
➔ Laryngeal nerve damage may occur during
surgery. This problem results in hoarseness.
Assess voice Q2H.
NONSURGICAL Mgt.: HYPERTHYROIDISM
➔ Monitor VS: Increases in temperature may
indicate a rapid worsening of the patient's
condition and the onset of thyroid storm
➔ Thyroid storm: is characterized by high fever and
severe hypertension.
➔ Drug therapy with antithyroid drugs is the initial
treatment for hyperthyroidism
➔ The preferred drugs are the thionamides,
especially methimazole (Tapazole).
➔ Methimazole can cause birth defects and should
not be used during pregnancy, especially during
the first trimester.
➔ Propylthiouracil (PTU) is used less often because
of its liver toxic effects
➔ Iodine preparations may be used for short-term
therapy before surgery. They decrease blood flow
through the thyroid gland, reducing the production
and release of thyroid hormones.
➔ Beta-adrenergic blocking drugs such as
propranolol (Inderal, Detensol ) may be used as
supportive therapy
INFLAMMATORY BOWEL DISEASE
● Ulcerative Colitis
➔ widespread inflammation of mainly the rectum
and rectosigmoid colon but can extend to the
entire colon when the disease is extensive.
➔ UC is a disease that is associated with periodic
remissions and exacerbations (flare-ups)
➔ Older adults with UC are at high risk for impaired
fluid and electrolyte balance as a result of
diarrhea, including dehydration and hypokalemia.
➔ The intestinal mucosa becomes hyperemic (has
increased blood flow), edematous, and reddened
➔ In more severe inflammation, the lining can
bleed and small erosions, or ulcers, occur.
Abscesses can form in these ulcerative areas
and result in tissue necrosis
➔ Continued edema and mucosal thickening can
lead to a narrowed colon and possibly a partial
bowel obstruction
➔ The patient's stool typically contains blood and
mucus. Patients report tenesmus (an unpleasant
and urgent sensation to defecate) and lower
abdominal colicky pain relieved with defecation.
➔ With long-term disease, cellular changes can
occur that increase the risk for colon cancer
➔ Abdominal pain, diarrhea, rectal bleeding, and
fecal urgency are common symptoms of
ulcerative colitis
➔ Anorexia, weight loss, cramping, vomiting, fever,
and dehydration associated with passing 5 to 20
liquid stools a day may also occur.
➔ Along with the potential for fluid and electrolyte
imbalance, there is a loss of calcium. Anemia
often develops as a result of rectal bleeding.
➔ Serum albumin may be low because of
malabsorption.
➔ Other complications include the potential for
hemorrhage during an acute phase, bowel
obstruction, perforation, and peritonitis
➔ The risk for colon cancer is also increased in
patients with ulcerative colitis.
➔ The diagnosis usually is confirmed by
sigmoidoscopy, colonoscopy, biopsy, and by
negative stool examinations for infectious or
other causes.
➔ Fiber supplements may be used to decrease
diarrhea and rectal symptoms.
➔ Surgical treatment (i.e., removal of the rectum
and entire colon) with the creation of an
ileostomy or ileoanal anastomosis may be
required for people who do not respond to
medications and conservative methods of
treatment.
➔ The medications used in treatment of ulcerative
colitis are similar to those used in the treatment
of Crohn disease. They include the
nonabsorbable 5-ASA compounds (e.g.,
mesalamine, olsalazine).
➔ The corticosteroids are used selectively to
lessen the acute inflammatory response
➔ Ulcerative colitis is characterized by
deoxyribonucleic acid (DNA) damage with
microsatellite instability in mucosa cells.
Crohn’s Disease
➔ Recurrent, granulomatous type of inflammatory
response
➔ Slowly progressive, relentless, and often disabling
disease.
➔ Common in: people in their twenties or thirties,
with women being affected slightly more often
than men.
➔ A characteristic feature of Crohn disease is the
sharply demarcated, granulomatous lesions that
are surrounded by normal-appearing mucosal
tissue
➔ .Skip lesions = multiple interspersed lesions
➔ All the layers of the bowel are involved, with the
submucosal layer affected to the greatest extent
➔ The surface of the inflamed bowel usually has a
characteristic “cobblestone” appearance
resulting from the fissures and crevices that
develop, surrounded by areas of submucosal
edema.
➔ The bowel wall, after a time, often becomes
thickened and inflexible; its appearance has been
likened to a lead pipe or rubber hose
➔ The adjacent mesentery may become inflamed,
and the regional lymph nodes and channels may
become enlarged.
Clinical Manifestations:
➔ The principal symptoms, which are dependent
upon the area of the GI system that is affected,
include diarrhea, abdominal pain, weight loss, fluid
and electrolyte disorders, malaise, and low-grade
fever
➔ Because Crohn disease affects the submucosal
layer to a greater extent than the mucosal layer,
there is less bloody diarrhea than with ulcerative
colitis
➔ The absorptive surface of the intestine may be
disrupted; nutritional deficiencies may occur,
related to the specific segment of the intestine
involved
➔ When Crohn disease occurs in childhood, one of
its major manifestations may be retardation of
growth and significant malnutrition.
Complications:
➔ Fistula formation = tubelike passages that form
connections between different sites in the GI tract
➔ Abdominal abscess formation
➔ Intestinal obstruction
Diagnosis:
➔ Sigmoidoscopy is used for direct visualization of
the affected areas and to obtain biopsies
➔ In people suspected of having Crohn disease,
radiographic contrast studies provide a means for
determining the extent of involvement of the
small bowel
➔ CT scans may be used to detect an inflammatory
mass or abscess.
Treatment:
➔ Treatment methods focus on terminating the
inflammatory response and promoting healing,
maintaining adequate nutrition, and preventing
and treating complications.
➔ corticosteroids, sulfasalazine, metronidazole,
azathioprine, 6-mercaptopurine, methotrexate,
and infliximab
➔ Agents containing 5-ASA affect multiple sites in
the arachidonic acid pathway critical to the
pathogenesis of inflammation. Sulfasalazine
contains 5-ASA with sulfapyridine linked to an
azo bond. The drug is poorly absorbed from the
intestine, and the azo linkage is broken down by
the bacterial flora in the ileum and colon to
release 5-ASA.
➔ Metronidazole is an antibiotic used to treat
bacterial overgrowth in the small intestine.
➔ A recent metaanalysis found two thiopurine
drugs, azathioprine and 6-mercaptopurine, to be
effective in reducing the reoccurrence of Crohn
disease
➔ The use of methotrexate is another option for
clinicians to choose instead of the thiopurine
drugs, although the studies regarding its use are
limited.
➔ Infliximab is a monoclonal antibody that targets
the destruction of tumor necrosis factor (TNF), a
mediator of the inflammatory response, whose
expression is increased in inflammatory
processes such as Crohn disease
➔ Nutritional deficiencies are common in Crohn
disease because of diarrhea, steatorrhea, and
other malabsorption problems.
➔ Because fats often aggravate the diarrhea, it is
recommended that they be avoided
➔ Total parenteral nutrition (i.e., parenteral
hyperalimentation) consists of intravenous
administration of hypertonic glucose solutions to
which amino acids and fats may be added
ADDISON’S DISEASE/ PRIMARY ADRENAL
CORTICAL INSUFFICIENCY
● Adrenal cortical hormones are deficient and ACTH
levels are elevated because of lack of feedback
inhibition.
● This disease is a relatively rare disorder in which
all the layers of the adrenal cortex are destroyed
● Drugs that inhibit synthesis or cause excessive
breakdown of glucocorticoids can also result in
adrenal insufficiency (e.g., ketoconazole).
Clinical Manifestations
➔ These manifestations are related primarily to
mineralocorticoid deficiency, glucocorticoid
deficiency, and hyperpigmentation resulting from
elevated ACTH levels.
- Although lack of the adrenal androgens (i.e.,
DHEAS) exerts few effects in men because
the testes produce these hormones, women
have sparse axillary and pubic hair.
➔ Mineralocorticoid deficiency causes increased
urinary losses of sodium, chloride, and water,
along with decreased excretion of potassium
➢ . The result is hyponatremia, loss of
extracellular fluid, decreased cardiac output,
and hyperkalemia. There may be an abnormal
appetite for salt. Orthostatic hypotension is
common. Dehydration, weakness, and fatigue
are common early symptoms.
➢ If loss of sodium and water is extreme,
cardiovascular collapse and shock ensue
➔ Glucocorticoid deficiency = poor tolerance to
stress
➢ This deficiency causes hypoglycemia, lethargy,
weakness, fever, and gastrointestinal symptoms
such as anorexia, nausea, vomiting, and weight
loss.
➔ elevated levels of ACTH = Hyperpigmentation
➔ The skin looks bronzed or suntanned in exposed
and unexposed areas, and the normal creases
and pressure points tend to become especially
dark. The gums and oral mucous membranes may
become bluish-black
Treatment
➔ Hydrocortisone is usually the drug of choice
➔ In mild cases, hydrocortisone alone may be
adequate. Fludrocortisone (a mineralocorticoid) is
used for persons who do not obtain a sufficient
salt-retaining effect from hydrocortisone.
➔ DHEAS replacement may also be helpful in the
female patient
➢ Because people with the disorder are likely to
have episodes of hyponatremia and
hypoglycemia, they need to have a regular
schedule for meals and exercise
➢ People with Addison disease also have limited
ability to respond to infections, trauma, and
other stresses.
➔ For acute adrenal insufficiency, the five Ss of
management should be followed: (1) Salt
replacement, (2) Sugar (dextrose) replacement,
(3) Steroid replacement, (4) Support of
physiologic functioning, and (5) Search for and
treat the underlying cause (e.g., infection)
DIABETES MELLITUS (refer to Dr. Baldomero’s
notes)
● Type 2 diabetes currently accounts for about 90%
to 95% of the cases of diabetes.
● Glucose is stored inside cells as glycogen in the
liver and muscles, and free fatty acids are stored
as triglyceride in fat cells.
● Fat is the most efficient means of storing energy,
with 9 calories of stored energy per gram
● Protein and carbohydrate have only 4 calories per
gram.
● In the liver, insulin promotes the production and
storage of glycogen (glycogenesis)
● Glycogenolysis: glycogen breakdown into
glucose
● Insulin inhibits ketogenesis = conversion of fats
to acids
● Gluconeogenesis = conversion of protein to
glucose
● In muscle, insulin promotes protein and glycogen
synthesis. In fat cells, it promotes triglyceride
storage.
3 CLASSIC MANIFESTATIONS:
➔ Polyuria is frequent and excessive urination and
results from an osmotic diuresis caused by
excess glucose in the blood and urine. With
diuresis, electrolytes are excreted in the urine
and water loss is severe.
➔ Polydipsia (excessive thirst) occurs
➔ Because the cells receive no glucose, cell
starvation triggers Polyphagia (excessive
eating). Despite eating, the person remains in
cellular starvation until insulin is available to
move glucose into the cells.
SIADH
Remember:
❏ The anterior pituitary gland regulates growth,
metabolism, and sexual development.
❏ The posterior pituitary gland secretes vasopressin
(antidiuretic hormone [ADH])
❏ ADH deficiency causes diabetes insipidus
❏ ADH excess causes the syndrome of
inappropriate antidiuretic hormone (SIADH).
● SIADH = aka Schwartz-Bartter syndrome
● Normally, ADH is secreted when more fluid
(water) is needed in the body, such as when
plasma volume is decreased
● Cancer is a common cause of SIADH, especially
small cell lung cancer.
● SIADH also may occur with other cancers,
including head and neck, melanoma,
gastrointestinal, prostate, and hematologic
malignancies, especially when tumors are present
in the brain
● Drugs often used in patients with cancer also can
cause SIADH (e.g., morphine sulfate,
cyclophosphamide).
● In SIADH, water is reabsorbed in excess by the
kidney and put into systemic circulation
● The retained water dilutes blood sodium levels =
dilutional hyponatremia
● Mild manifestations include weakness, muscle
cramps, loss of appetite, and fatigue
● Fluid Retention = weight gain, nervous system
changes, personality changes, confusion, and
extreme muscle weakness occur
● As the sodium level drops toward 110 mEq/L,
seizures, coma, and death may follow
NURSING PRIORITIES
➔ patient safety, restoring normal fluid balance, and
providing supportive care
➔ Management includes fluid restriction, increased
sodium intake, and drug therapy
➔ One drug, demeclocycline (Declomycin), works
in opposition to ADH
➔ Effective treatment of the cancer triggering the
syndrome is the only cure for SIADH.

Safety Priority!
➔ Monitor for increasing fluid overload
(bounding pulse, increasing neck vein distention
(jugular venous distention [JVD]), presence of
crackles in lungs, increasing peripheral edema,
reduced urine output) at least every 2 hours.
➔ Pulmonary edema can occur very quickly and
can lead to death.
➔ In SIADH, ADH continues to be released even
when plasma is hypoosmolar, leading to
disturbances of fluid and electrolyte balance.
➔ The increase in blood volume increases the
kidney filtration and inhibits the release of renin
and aldosterone, which increase urine sodium
loss and leads to greater hyponatremia.
DIAGNOSIS:
➔ Radioimmunoassay of ADH along with clinical
manifestations can help diagnose SIADH, but
this test is usually not used for a definitive
diagnosis.
MANAGEMENT
➔ Drug therapy with tolvaptan (Samsca) or
conivaptan (Vaprisol) is used to treat SIADH
when hyponatremia is present in hospitalized
patients
➢ Tolvaptan is an oral drug, and conivaptan is
given IV
➢ !!! Tolvaptan has a black box warning that
rapid increases in serum sodium levels (those
greater than a 12 mEq/L increase in 24 hours)
have been associated with central nervous
system demyelination that can lead to serious
complications and death formation:
➢ when this drug is used at higher dosages or
for longer than 30 days, there is a significant
risk for liver failure and death
➔ Medical interventions for SIADH focus on
restricting fluid intake, promoting the excretion of
water, replacing lost sodium, and interfering with
the action of ADH.
➔ Fluid restriction is essential because fluid intake
further dilutes plasma sodium levels. In some
cases, fluid intake may be kept as low as 500 to
1000 mL/24 hr Predisposing Factors: 5 F’s
➔ Dilute tube feedings with saline rather than water,
and use saline to irrigate GI tubes. Mix drugs to
be given by GI tube with saline.
➔ MONITOR WEIGHT = A 2.2-lb (1kg) weight
increase is equal to a 1000-mL fluid retention (1
kg = 1 L).
➔ Diuretics may be used to manage SIADH when
sodium levels are near normal and heart failure is Pathophysiology
present
➔ For milder SIADH, demeclocycline
(Declomycin), an oral antibiotic, may help correct
the disturbed fluid and electrolyte balance
➔ Hypertonic saline (i.e., 3% sodium chloride [3%
NaCl]) may be used to treat SIADH when the
serum sodium level is very low
CHOLELITHIASIS WITH CHOLECYSTITIS
● Cholelithiasis is the presence of gallstones
(formed by hardening or adherence of
particles of bile constituents).
● Acute cholecystitis is an inflammation of the
gallbladder that may occur with cholelithiasis.
Four theories that attempt to explain gallstone
1. Bile may undergo a change in composition -
bile is saturated with cholesterol (that will
precipitate to form stones) but deficient in bile
salts.
2. Gallbladder stasis may lead to bile stasis
which may change the composition of bile.
3. Infection - inflammatory debris can form a
point of origin for stone formation.
4. Genetics and demography
Female
Fat (high intake of fat)
Fair (Caucasian)
Forty
Fertile (multigravida and those using
contraceptive pills)
● The gallstone causes pressure within the
gallbladder.
● As the gallstone continues to increase in size,
obstruction to bile flow occurs.
● Bile stasis occurs due to obstruction of bile
flow.
● Bile stasis leads to the following:
➔ Decreased fat emulsification
Manifestations:
1. Fat intolerance
2. Anorexia
3. Nausea and vomiting
4. Weight loss
5. Gaseous eructation (belching)
6. Flatulence, bloating
 7. Steatorrhea
➔ Inflammation of the gallbladder
Manifestations:
1. Pain - epigastric pain that radiates to the
scapula 2-4 hours after eating fatty foods and
may persist for 4-8 hours. Then, pain becomes
localized in RUQ with guarding and rigidity.
2. Fever, leukocytosis
3. Murphy’s sign - client cannot take a deep
breath when the examiner’s fingers are
passed below the hepatic margin
➔ Biliary obstruction/Decreased bile flow into
the colon
Manifestations:
1. Acholic stool (pale/gray/clay-colored stool)
2. Decreased Vit K absorption leading to
bleeding tendencies
3. Increased serum bilirubin leading to jaundice,
pruritus, and tea-colored urine
➔ Infection - cholecystitis and pancreatitis may
occur
Collaborative Management
1. Relief of pain
● Administer analgesic. Meperidine HCl
(Demerol) is the drug of choice.
● Avoid morphine sulfate as it causes
spasm of Sphincter of Oddi (may
increase pain)
● Administer anticholinergic to relax
smooth muscles.
2. Diet
● During episodes of nausea and
vomiting, maintain NPO with IV fluids.
● Small, frequent feedings
● Avoid gas-forming foods
3. Administer antiemetics for nausea and
vomiting
4. Administer medications for cholelithiasis
(gallstone dissolution)
a. Chenodeoxycholic Acid (Chenix) -
decreases cholesterol production,
lowering content of bile, and facilitates
dissolution of gallstones
● Hepatotoxic; baseline liver
function studies should be
performed
● May cause diarrhea
● Administer with food or milk
● Avoid aluminum-containing
substances
b. Ursodiol (Actigall) - inhibits absorption
of cholesterol and facilitates dissolution
of gallstone (requires months of
therapy)
● Administer with food or milk
● Avoid aluminum-containing
substances
c. Monoctanoid (Moctatin) - used when
stones made of calcium are resistant to
dissolution by orally administered
chenodiol
● Administered through a T-tube, biliary
catheter, or percutaneous transhepatic
catheter for direct contact with the stone.
Note: Major side effects of medications for
cholelithiasis are abdominal pain, diarrhea, nausea
and vomiting.
5. Extracorporeal shockwave lithotripsy - to
disintegrate stones in the biliary system. Oral
dissolution then follows.
6. Surgical interventions
Cholecystectomy - removal of the gallbladder;
laparoscopic or incisional/open
Pre-op care:
● For incisional/open cholecystectomy, teach
the client deep breathing, coughing, and
turning (DBCT) exercises
● If prothrombin time is prolonged during this
period, the client with receive Vit K injection to
prevent bleeding
Post-op care:
● Position the client in semi-Fowler’s to promote
lung expansion
● NGT is in place to drain gastric content and
prevent abdominal distention
● Reinforce DBCT exercises to prevent
respiratory complications
● Diet: Low-fat for 2-3 months then gradually
introduce fats according to tolerance
● Early ambulation is encouraged to prevent
post-op complications
● In open cholecystectomy, the client will have a
T-tube in place during the post-op period.
Purposes of the T-tube:
1. To drain bile from the common bile
duct and minimize amount of bile
flowing into the duodenum
2. To maintain patency of the common
bile duct which may be swollen for the
first few days post-op
3. To prevent leakage of bile into the
peritoneum and prevent bile peritonitis
➔ The normal color of drainage from the T-tube
for the first 24 hours is reddish brown. After
24 hours, it becomes green-brown.
 ➔ The normal amount draining from the T-tube
during the first 24 hours postop is 300-500 ml;
then up to 500-1000 ml per day after 24 hours
➔ The drainage bottle should be placed in bed,
below the level of the gallbladder. This allows
drainage of excess bile, not all of the bile.
DIABETES MELLITUS
Prediabetes
● Prediabetes is defined as impaired glucose
tolerance (IGT), impaired fasting glucose (IFG), or
both.
● A diagnosis of IGT is made if the 2-hour oral
glucose tolerance test (OGTT) values are 140 to
199 mg/dL (7.8 to 11.0 mmol/L)
● IFG is diagnosed when fasting blood glucose
levels are 100 to 125 mg/dL (5.56 to 6.9 mmol/L).
Clinical Manifestations:
● The classic symptoms are polyuria, polydipsia,
and polyphagia. The osmotic effect of glucose
produces the manifestations of polydipsia and
polyuria. Polyphagia is a consequence of cellular
malnourishment when insulin deficiency prevents
utilization of glucose for energy. Weight loss may
occur because the body cannot get glucose and
turns to other energy sources, such as fat and
protein.
● Some of the more common manifestations
associated with type 2 diabetes are fatigue,
recurrent infections, recurrent vaginal yeast or
candidal infections, prolonged wound healing, and
visual changes.
DIAGNOSTIC TESTS:
1. A1C of 6.5% or higher.
2. Fasting plasma glucose (FPG) level greater than or
equal to 126 mg/dL (7.0 mmol/L). Fasting is defined
as no caloric intake for at least 8 hours.
3. Two-hour plasma glucose level greater than or
equal to 200 mg/dL (11.1 mmol/L) during an OGTT,
using a glucose load of 75 g.
4. In a patient with classic symptoms of
hyperglycemia (polyuria, polydipsia, unexplained
weight loss) or hyperglycemic crisis, a random plasma
glucose greater than or equal to 200 mg/dL (11.1
mmol/L)
➔ A1C measures the amount of glycosylated
hemoglobin as a percentage of total hemoglobin
(e.g., A1C of 6.5% means that 6.5% of the total
hemoglobin has glucose attached to it)
➔ The A1C has several advantages over the FPG,
including greater convenience, since fasting is not
required
➔ Diseases affecting RBCs (e.g., iron deficiency
anemia or sickle cell anemia) can influence the
A1C and should be considered when interpreting
test results
➔ Fructosamine can also be used to assess
glucose control. Fructosamine is formed by a
chemical reaction of glucose with plasma protein.
It reflects glucose control in the previous 1 to 3
weeks. Fructosamine levels may show a change
in glucose control before A1C does.
➔ Islet cell autoantibody testing is primarily
ordered to help distinguish between autoimmune
type 1 diabetes and diabetes from other causes.
Autoantibodies can develop to one or several of
the autoantigens—GAD65, IA-2, or insulin.
MANAGEMENT:
● The three major types of glucose-lowering agents
(GLAs) used in the treatment of diabetes are
insulin, oral agents (OAs), and noninsulin
injectable agents
➔ All individuals with type 1 diabetes require insulin.
➔ For some people with type 2 diabetes, a regimen
of proper nutrition, regular physical activity, and
maintenance of desirable body weight is sufficient
to attain optimal blood glucose control. However,
eventually most people with type 2 diabetes will
require medication management because
diabetes is a progressive disease.
Drug therapy: INSULIN
➔ The insulin is derived from common bacteria
(e.g., Escherichia coli) or yeast cells using
recombinant deoxyribonucleic acid (DNA)
technology
➔ In the past, insulin was extracted from beef and
pork pancreas, but their use was associated with
high rates of allergic reactions and complications.
These forms of insulin are no longer available.

Mealtime Insulin bolus
● Rapid-acting synthetic insulin analogs, which
include lispro (Humalog), aspart (NovoLog), and
glulisine (Apidra), have an onset of action of
approximately 15 minutes and should be injected
within 15 minutes of mealtime.
➔ The rapid-acting analogs most closely mimic
natural insulin secretion in response to a meal.
● Short-acting regular insulin has an onset of
action of 30 to 60 minutes and should be injected
30 to 45 minutes before a meal to ensure that the
onset of action coincides with meal absorption
➔ Short-acting insulin is also more likely to cause
hypoglycemia because of a longer duration of
action.
● Long or intermediate-acting Insulin
➔ Many people with type 2 diabetes who use oral
medications also require insulin to adequately
control blood glucose levels.
➔ The long-acting insulins, glargine (Lantus) and
detemir (Levemir), are often added to the
medication regimen
➔ This type of insulin is released steadily and
continuously, and for most people do not have a
peak of action
➔ Because they lack peak action time, the risk for
hypoglycemia from this type of insulin is greatly
reduced.
➔ Intermediate-acting insulin (NPH) is also used
as a basal insulin. It has a duration of 12 to 18
hours. The disadvantage of NPH is that it has a
peak ranging from 4 to 12 hours, which can result
in hypoglycemia.
➔ NPH is a cloudy insulin that must be gently
agitated before administration.
Storage of Insulin
1. Insulin vials and insulin pens currently in use
may be left at room temperature for up to 4
weeks unless the room temperature is higher
than 86° F (30° C) or below freezing (less than
32° F [0° C])
2. Prolonged exposure to direct sunlight should be
avoided.
3. Prefilled syringes containing two different
insulins are stable for up to 1 week when stored
in the refrigerator, whereas syringes containing
only one type of insulin are stable up to 30
days.1
4. Syringes should be stored in a vertical position
with the needle pointed up to avoid clumping of
suspended insulin in the needle.
5. Before injection, gently roll prefilled syringes
between the palms 10 to 20 times to warm the
insulin and resuspend the particles.
Administration of Insulin
● The fastest subcutaneous absorption is from the
abdomen, followed by the arm, thigh, and
buttock.
● Caution the patient about injecting into a site
that is to be exercised
- Exercise of the injection site, together with the
increased body heat and circulation generated
by the exercise, may increase the rate of
absorption and speed the onset of insulin
action.
● Teach patients to rotate the injection within one
anatomic site, such as the abdomen, for at least
1 week before using a different site, such as the
right thigh. This allows for better absorption.
➔ Injections are rotated systematically across the
area, with each injection site at least 1/2 to 1 in
away from the previous injection site.
Problems with Insulin Therapy:
1. Allergic Reactions - Local inflammatory
reactions to insulin may occur, such as itching,
 erythema, and burning around the injection
site.
- Zinc or protamine used as a preservative in
the insulin and the latex or rubber stoppers on
the vials have been implicated in allergic
reactions
2. Lipodystrophy - (atrophy of subcutaneous
tissue) may occur if the same injection sites
are used frequently.
- The use of hypertrophied sites may result in
erratic insulin absorption
3. Somogyi Effect & Dawn Phenomenon
- Somogyi Effect: A high dose of insulin
produces a decline in blood glucose levels
during the night. As a result, counterregulatory
hormones (e.g., glucagon, epinephrine, growth
hormone, cortisol) are released, stimulating
lipolysis, gluconeogenesis, and
glycogenolysis, which in turn produce rebound
hyperglycemia.
- If a patient is experiencing morning
hyperglycemia, checking blood glucose levels
between 2:00 and 4:00 AM for hypoglycemia
will help determine if the cause is the Somogyi
effect.
- headaches on awakening and having night
sweats or nightmares. A bedtime snack, a
reduction in the dose of insulin, or both can
help to prevent the Somogyi effect
● Dawn phenomenon is also characterized by
hyperglycemia that is present on awakening. It
has been suggested that two counterregulatory
hormones, growth hormone and cortisol, excreted
in increased amounts in the early morning hours
are responsible.
- The dawn phenomenon affects a majority of people
with diabetes and tends to be most severe when
growth hormone is at its peak in adolescence and
young adulthood.
➔ The treatment for Somogyi effect is less insulin.
The treatment for dawn phenomenon is an
increase in insulin or an adjustment in
administration time
Oral & Noninsulin Injectable Agents
These drugs work on three defects of type 2 diabetes:
1) insulin resistance
2) decreased insulin production
3) increased hepatic glucose production.
● Biguanides
➔ The most widely used oral diabetes agent is
metformin. The primary action of metformin is
to reduce glucose production by the liver. It
also enhances insulin sensitivity at the tissue
level and improves glucose transport into the
cells. Additionally, it has beneficial effects on
plasma lipids.
➔ Metformin is the first-choice drug for most
people with type 2 diabetes.
➔ Patients who are undergoing surgery or any
radiologic procedures that involve the use of a
contrast medium are instructed to temporarily
discontinue metformin before surgery or the
procedure. They should not resume the metformin
until 48 hours afterward, once their serum
creatinine has been checked and is normal.
➔ IV contrast media that contain iodine pose a risk
of acute kidney injury, which could exacerbate
metformin-induced lactic acidosis.
● Sulfonylureas
➔ Sulfonylureas include glipizide (Glucotrol,
Glucotrol XL), glyburide (Micronase, DiaBeta,
Glynase), and glimepiride (Amaryl).
➔ The primary action of the sulfonylureas is to
increase insulin production by the pancreas.
Therefore hypoglycemia is the major side effect
with sulfonylureas.
● Meglitinides
➔ Like the sulfonylureas, repaglinide (Prandin) and
nateglinide (Starlix) increase insulin production by
the pancreas.
➔ However, because they are more rapidly
absorbed and eliminated than sulfonylureas, they
are less likely to cause hypoglycemia.
➔ Instruct patients to take meglitinides any time
from 30 minutes before each meal right up to the
time of the meal. These drugs should not be taken
if a meal is skipped.
● Alpha-glucosidae inhibitors
➔ Also known as “starch blockers,” these drugs work
by slowing down the absorption of carbohydrate in
the small intestine.
➔ Acarbose (Precose) and miglitol (Glyset) are the
available drugs in this class.
➔ Taken with the first bite of each main meal, they
are most effective in lowering postprandial blood
glucose.
➔ AGIs delay absorption of glucose from GI tract
● Thiazolidinediones
➔ Sometimes referred to as “insulin sensitizers,”
these agents include pioglitazone (Actos) and
rosiglitazone (Avandia).
➔ Increase glucose uptake in muscle; decrease
endogenous glucose production.
➔ They are most effective for people who have
insulin resistance
➔ These agents improve insulin sensitivity,
transport, and utilization at target tissues.
Because they do not increase insulin production,
thiazolidinediones do not cause hypoglycemia
when used alone.
➔ rarely used today because of their adverse
effects.
➔ Rosiglitazone is associated with adverse
cardiovascular events
➔ Pioglitazone can worsen heart failure and is
associated with an increased risk of bladder
cancer.
● Dipeptidyl Peptidase-4 (DPP-4) inhibitors
➔ Incretin hormones are released by the intestines
throughout the day, but levels increase in
response to a meal.
➔ When glucose levels are normal or elevated,
incretins increase insulin synthesis and release
from the pancreas, as well as decrease hepatic
glucose production. The incretin hormones are
normally inactivated by dipeptidyl peptidase-4
(DPP-4).
● Sodium-Glucose Co-Transporter 2 (SGLT2)
Inhibitors
➔ Canagliflozin (Invokana) is the first drug in a new
class of drugs known as sodium-glucose co-
transporter 2 (SGLT2) inhibitors.
➔ It works by blocking the reabsorption of glucose
by the kidney, increasing glucose excretion, and
lowering blood glucose levels in diabetics.
● Dopamine Receptor Agonist
➔ Bromocriptine (Cycloset) is a dopamine receptor
agonist that improves glycemic control.
➔ The mechanism of action is unknown. Patients
with type 2 diabetes are thought to have low levels
of dopamine activity in the morning. These low
levels of dopamine may interfere with the body’s
ability to control blood glucose.
➔ Bromocriptine increases dopamine receptor
activity. It can be used alone or as an add-on to
another type 2 diabetes treatment.
● Glucagon-like Peptide Receptor Agonist
➔ Exenatide (Byetta), exenatide extended-release
(Bydureon), and liraglutide (Victoza) simulate
GLP-1 (one of the incretin hormones), which is
found to be decreased in people with type 2
diabetes.
➔ These drugs increase insulin synthesis and
release from the pancreas, inhibit glucagon
secretion, decrease gastric emptying, and reduce
food intake by increasing satiety.
● Amylin Analog
➔ Pramlintide (Symlin) is the only available amylin
analog. Amylin, a hormone secreted by the β cells
of the pancreas in response to food intake, slows
gastric emptying, reduces glucagon secretion, and
increases satiety
➔ Pramlintide is used in addition to mealtime insulin
in patients with type 1 or type 2 diabetes who do
not have good glucose control on ideal insulin
therapy.
➔ It is only used concurrently with insulin and is not
a replacement for insulin
➔ Pramlintide is administered before major meals
subcutaneously into the thigh or abdomen. It
cannot be injected into the arm because
absorption from this site is too variable. The drug
cannot be mixed in the same syringe with insulin.
➔ The concurrent use of pramlintide and insulin
increases the risk of severe hypoglycemia during
the 3 hours after injection, especially in patients
with type 1 diabetes
➔ Instruct patients to eat a meal with at least 250
calories and keep a form of fast acting glucose on
hand in the event that hypoglycemia develops.
When pramlintide is used, the bolus dose of
insulin should be reduced.
➔ Pramlintide (Symlin) can cause severe
hypoglycemia when used with insulin
OTHER DRUGS AFFECTING GLUCOSE LEVELS
➔ β-adrenergic blockers can mask symptoms of
hypoglycemia and prolong the hypoglycemic
effects of insulin.
➔ Thiazide and loop diuretics can potentiate
hyperglycemia by inducing potassium loss
Diabetic Ketoacidosis
➔ is caused by a profound deficiency of insulin and
is characterized by hyperglycemia, ketosis,
acidosis, and dehydration.
➔ It is most likely to occur in people with type 1
diabetes but may be seen in people with type 2
diabetes in conditions of severe illness or stress
when the pancreas cannot meet the extra
demand for insulin.
➔ Precipitating factors include illness and infection,
inadequate insulin dosage, undiagnosed type 1
diabetes, poor self-management, and neglect
➔ When the circulating supply of insulin is
insufficient, glucose cannot be properly used for
energy. The body compensates by breaking
down fat stores as a secondary source of fuel
➔ Ketones are acidic by-products of fat metabolism
that can cause serious problems when they
become excessive in the blood
➔ Ketosis alters the pH balance, causing metabolic
acidosis to develop. Ketonuria is a process that
occurs when ketone bodies are excreted in the
urine. During this process, electrolytes become
depleted as cations are eliminated along with the
anionic ketones in an attempt to maintain
electrical neutrality.
➔ Insulin deficiency impairs protein synthesis and
causes excessive protein degradation. This
results in nitrogen losses from the tissues. Insulin
deficiency also stimulates the production of
glucose from amino acids (from proteins) in the
liver and leads to further hyperglycemia. Because
of the deficiency of insulin, the additional glucose
cannot be used and the blood glucose level rises
further, adding to the osmotic diuresis.
➔ If not treated, the patient will develop severe
depletion of sodium, potassium, chloride,
magnesium, and phosphate.
➔ Vomiting caused by the acidosis results in more
fluid and electrolyte losses. Eventually,
hypovolemia followed by shock will ensue. Renal
failure, which may eventually occur from
hypovolemic shock, causes the retention of
ketones and glucose, and the acidosis
progresses
➔ Untreated, the patient becomes comatose as a
result of dehydration, electrolyte imbalance, and
acidosis. If the condition is not treated, death is
inevitable.
Clinical Manifestations: DKA
➔ Dehydration occurs in DKA with manifestations of
poor skin turgor, dry mucous membranes,
tachycardia, and orthostatic hypotension.
➔ Early symptoms may include lethargy and
weakness. As the patient becomes severely
dehydrated, the skin becomes dry and loose, and
the eyes become soft and sunken.
➔ Abdominal pain may be present and
accompanied by anorexia, nausea, and vomiting
➔ Kussmaul respirations (rapid, deep breathing
associated with dyspnea) are the body’s attempt
to reverse metabolic acidosis through the
exhalation of excess carbon dioxide.
➔ Acetone is noted on the breath as a sweet, fruity
odor
➔ Laboratory findings include a blood glucose level
greater than or equal to 250 mg/dL (13.9
mmol/L), arterial blood pH less than 7.30, serum
bicarbonate level less than 16 mEq/L (16
mmol/L), and moderate to large ketones in the
urine or serum.
Interventions for DKA:
• Ensure patent airway.
•Administer O2 via nasal cannula or non-rebreather
mask.
•Establish IV access with large-bore catheter.
•Begin fluid resuscitation with 0.9% NaCl solution 1
L/hr until BP stabilized and urine output 30-60 mL/hr.
• Begin continuous regular insulin drip 0.1 U/kg/hr.
• Identify history of diabetes, time of last food, and
time and amount of last insulin injection.
• Administer sodium bicarbonate if severe acidosis
(pH <7.0).
LIVER CIRRHOSIS
● Chronic progressive disease of the liver
characterized by diffuse damage to cells with
fibrosis and nodular regeneration.
● Causes are as follows: alcohol abuse (most
common), malnutrition, infection, drugs, biliary
obstruction, and right-sided congestive heart
failure
● These factors lead to destruction of
hepatocytes, leading to fibrosis/scarring.
● Fibrosis and scarring of the liver may cause:
1. Obstruction of blood flow within the
liver
2. Increased pressure in the portal vein
and sinusoidal channels
3. Fatty infiltration of the liver (if cirrhosis
is alcohol-induced)
● These 3 factors eventually lead to portal
hypertension which is persistent increase in
pressure within the portal vein that develops
as a result of obstruction to blood flow.
Clinical Manifestations
1. Anorexia, weakness, weight loss - Anorexia is
an initial manifestation to liver function
impairment. These signs and symptoms of
malnutrition are due to inability of the liver to
metabolize nutrients and store fat-soluble
vitamins (ADEK).
2. Fever - normal physiologic response to liver
tissue damage
3. Jaundice, pruritus, tea-colored urine. These
are due to increased serum bilirubin levels.
Pruritus results from accumulation of bile salts
in the skin.
4. Bleeding - decreased synthesis of bile salts in
the liver prevents absorption of fat-soluble
vitamins. Decreased vitamin K absorption
results to reduced synthesis of clotting factors.
The client becomes prone to bleeding.
5. Decreased resistance to infection - due to the
destruction of Kupffer cells. Kupffer cells are
unable to perform phagocytosis.
6. Small, nodular liver - due to progressive
damage to the liver cells with fibrosis and
nodular regeneration
7. In males, the following manifestations occur
due to elevated estrogen levels in the blood:
a. Gynecomastia - enlargement of the
breast
b. Decreased libido - decrease in sexual
desire and stimulation
c. Impotence - erectile dysfunction
d. Fall of body hair
e. Atrophy of testicles - reduction in size
of the testicles
8. In females, the following manifestations occur
due to elevated androgen levels in the blood:
a. Hirsutism - excessive growth of body
hair
b. Acne
c. Deepening of voice
d. Increased virilism - having an
appearance of a male
9. Asterixis (liver flap) - a course tremor
characterized by rapid, nonrhythmic extension
and flexion on the wrist and fingers. This
results from neurologic function impairment
due to elevated serum ammonia levels.
10. Hepatic encephalopathy - this is end-stage
hepatic failure and cirrhosis caused by
elevated serum ammonia. Characterized by:
a. Confusion/disorientation
b. Delirium/hallucination
c. Fetor hepaticus - fruity, musty breath
odor of chronic liver disease
d. Hepatic coma - irreversible
11. Hepatorenal syndrome - progressive renal
failure associated with hepatic failure
characterized by:
a. Sudden decrease in urinary output
b. Elevated blood urea nitrogen and
creatinine
c. Decreased urine sodium excretion
d. Increased urine osmolarity
12. Portal hypertension leads to:
a. Hepatosplenomegaly - liver and spleen
become congested with blood
b. Caput medusae - dilated veins over the
abdomen
c. Spider angioma (telangiectasia) -
dilated capillaries over the face and
anterior neck. Also due to elevated
serum estrogen levels in males which
result from inability of the liver to
excrete adrenal cortex hormones,
including sex hormones
d. Palmar erythema - reddish palms. Also
due to elevated serum estrogen levels
in males
e. Ascites - accumulation of fluid within
the peritoneal cavity. It results from
venous congestion of the hepatic
capillaries. Capillary congestion leads
to plasma leaking directly from the liver
surface and portal vein. Ascites is also
due to hypoalbuminemia. The liver is
unable to metabolize protein
adequately. This results to decreased
colloidal osmotic pressure, causing
shifting of plasma from hepatic
capillaries into the peritoneal cavity.
f. Esophageal varices - fragile, thin-
walled, distended esophageal veins
that may become irritated and
ruptured. Portal hypertension causes
blood to circumvent to collateral
circulation like the esophageal veins
which are small and can easily become
varicosed (dilated)
g. Internal hemorrhoids, leg varicosities,
dependent edema - portal
hypertension causes venous stasis.
This leads to dilatation of veins in the
anal canal and legs, and shifting of
plasma from leg varicosities leads to
dependent edema.
Collaborative Management
1. Promote rest - to reduce metabolic demands
on the liver and maximize liver function
2. Diet should be high in calorie (2,000-
3,000/day) and high in carbohydrates to
maintain weight. Ample protein to rebuild
tissue but not high protein because this may
precipitate hepatic encephalopathy. Fat
restriction may be necessary during
progressive stage of the disease to prevent
fatty infiltration of the liver. Provide
 supplements of vitamins A, D, E, K, B-
complex, and C.
3. Skin care to relieve pruritus:
a. Wash the skin with warm water and
mild soap
b. Change position at regular intervals
c. Change linens and gowns as
necessary
d. Keep the environment cool: Sweating
intensifies pruritus.
e. Apply antipruritic agent on the skin as
prescribed (e.g. calamine lotion)
f. Administer oral cholestyramine resin (a
bile acid sequestrant, which enhances
excretion of bile salt via the feces), or
phenobarbital as prescribed
4. Prevent trauma or injury to prevent bleeding:
a. Monitor the client for bleeding gums,
melena, hematoma, purpura, and
hematemesis
b. Avoid or minimize parenteral injections;
use small gauge needle.
c. Apply pressure at injection site for 5
minutes.
d. Avoid rigorous nose blowing.
5. Protect client from infection - practice asepsis.
6. Minimize shortness of breath due to ascites by
elevating head of bed.
7. Relieve ascites:
a. Monitor daily weights, I&O, abdominal
girth
b. Restrict sodium and fluid intake
c. Administer diuretic as prescribed.
DOC: Spironolactone (Aldactone), a
potassium-sparing diuretic. In liver
cirrhosis, the liver is unable to excrete
adrenal cortex hormones including
aldosterone. As aldosterone level is
elevated, potassium is excreted (client
experiences hypokalemia)
d. To prevent hyperkalemia due to
Aldactone therapy, Furosemide (Lasix),
a potassium-wasting diuretic, may also
be prescribed.
e. Albumin IV may be prescribed to
increase colloidal osmotic pressure
and prevent shifting of plasma into the
peritoneal cavity (ascites). Also to
manage hypoalbuminemia.
f. Assist the client during paracentesis
(aspiration of fluid from the peritoneal
cavity)
g. LeVeen peritoneo-venous shunt is
used for clients with chronic ascites.
8. Prevent rupture of esophageal varices.
a. Advise client to avoid: screaming,
shouting, and yelling. Straining at
stools (administer stool softeners as
prescribed). Hot/spicy, rough foods.
Bending, stooping. Coughing,
sneezing.
b. Administer Propranolol (Inderal) to
reduce portal hypertension.
9. Control hemorrhage due to ruptured
esophageal varices:
a. Monitor BP, pulse, respiration, and
urine output continuously.
b. Administer IV fluids, plasma
expanders, and blood transfusions as
prescribed.
c. Administer vasopressin IV as
prescribed to lower portal pressure and
promote vasoconstriction.
d. Administer beta-adrenergic blocking
agents (propranolol, metoprolol, etc)
e. Balloon tamponade: Sengstaken-
Blakemore tube or Minnesota tube is
inserted by physician into the stomach
and he inflates the esophageal and
gastric balloons. Have scissors ready
at the bedside in order to remove the
tube in an emergency.
f. Sclerotherapy - an endoscope is
passed into the esophagus and a
sclerosing agent (e.g. morrhuate
sodium) is introduced into the varices
g. Portasystemic shunt - reduces portal
hypertension by sending portal venous
blood supply directly into the inferior
vena cava, bypassing the liver. This
reduces danger of hemorrhage from
varices.
10. Reduce ammonia formation to prevent hepatic
encephalopathy:
a. Lactulose (Chronulac, Duphalac) -
decreases the pH of the colon,
decreases production of alkaline
ammonia, and facilitates the excretion
of ammonia; s/e is 2-4 watery stools
per day. If more than 4 watery stools,
notify the physician.
b. Neomycin (Mycifradin) - reduce
colonic bacteria which are responsible
for the production of ammonia
c. Tap water or normal saline enema - to
remove digested blood from the colon,
following a period of bleeding into the
GIT. Because blood is protein, this
process increases ammonia in the gut
 and bloodstream. In turn, the excessive
ammonia disturbs brain function.
11. Avoid medications such as narcotics,
sedatives, barbiturates, acetaminophen.
These are hepatotoxic medications.
12. Avoid ASA, to prevent bleeding.
13. Most important client teaching: Avoid alcohol.