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PITUITARY GLAND
-Abnormalities of the anterior and posterior portion of the gland may occur independently
-Hypofunction of the pituitary gland (hypopituitarism) can result from disease of the pituitary gland
itself or of the hypothalamus (result is essentially the same)
-hypopituitarism can result from radiation therapy to the head + neck
-Total destruction of pituitary gland (ex. by trauma or tumor) removes all stimuli that are normally received by thyroid,
gonads, and adrenal glands. Result is extreme weight loss, emaciation, atrophy of all endocrine glands + organs, hair
loss, impotence, amenorrhea, hypometabolism, and hypoglycemia…Coma + death occur if missing hormones are not
replaced
ANTERIOR PITUITARY
-TSH, ACTH, FSH, and LH release hormones from other endocrine glands
-Prolactin acts on the breast to stimulate milk production
-GH protein hormone that increases protein synthesis in many tissues, increases the breakdown of
fatty acids in adipose tissue, and increases the glucose level in the blood (these actions of GH are
essential for normal growth)
Oversecretion:
• ACTH (Cushing’s)
• “Cushing’s syndrome – elevated cortisol level; blood sugar may be high”
• Basophilic tumors giv
• rise to Cushing syndrome with features highly attributable to hyperadrenalism, including masculinization and
amenorrhea in females, truncal obesity, HTN, osteoporosis, and polycythemia
• GH (acromegaly)
• Acromegaly = excess of GH in adults, results in enlargement of peripheral body parts without an increase in height
• Oversecretion of GH in children results in gigantism, person may grow up to 7 or 8 feet tall
• “Acromegaly – hypersecretion of GH; everything will be overdeveloped
– a lot of cardiac complications *
– sometimes they cannot see properly
– enlarged extremities, forehead
– female – might have issues with periods, anuria, or unable to have babies”
•
• Eosinophilic tumors that develop early in life result in gigantism – person may be over 7 ft. tall + large in all
proportions, but so weak + lethargic that can barely stand. If the disorder begins during adult life, the
excessive skeletal growth occurs only in the feet, hands, superciliary ridge, molar eminences, nose, chin,
giving rise to ACROMEGALY.
Insufficient secretion:
– GH (dwarfism)
• Dwarfism = insufficient secretion of GH during childhood results in generalized limited growth
• “Dwarfism – undersecretion of GH; other glands will be underdeveloped”
– Panhypopituitarism undersecretion commonly involving all of the anterior pituitary hormones
• Atrophy (shrining) of the thyroid gland, adrenal cortex, & gonads (b/c of loss of the tropic-
stimulating hormones)
• “everything is going to be decreased/diminished as a result”
POSTERIOR PITUITARY
- vasopressin (ADH) + oxytocin = hormones secreted by posterior lobe of pituitary gland; stored in the
post. pit. but synthesized in the hypothalamus
- ADH = controls excretion of water by the kidney; ADH secretion is stimulated by: an increase in
osmolality of the blood or be a decrease in BP
- Oxytocin – secretion is stimulated during pregnancy + childbirth; facilitates milk ejection during
lactation & increases contractions during labor + delivery
DIABETES INSIPIDUS
Patho: Deficiency of ADH decreases the collecting and distal renal tubules ability
to concentrate urine excessive diluted urine, excessive thirst, & excessive fluid intake
“kidney is going to be affected by this lack of vasopressin
patients will be very thirsty l require a lot of water b/c losing a lot of urine
Causes: may occur following surgical TX of a brain tumor, secondary to nonsurgical brain
tumors, traumatic brain injury, infections of the nervous system, post hypophysectomy,
failure of renal tubules to respond to ADH, and use of specific meds
Risk Factors:
o Head injuries and infections
o Lithium* or demeclocycline use
*TQ: Lithium affects vasopressin, has a relationship with this hormone
Google: Nephrogenic diabetes insipidus (NDI) is the most common renal side effect of lithium
therapy
Another cause of DI is failure of the renal tubules to rescond to ADH; this Nechrogenic form may
be related to hycokalemia, hycercalcemia, and a variety of medications (ex. lithium or
demeclocycline)
Clinical manifestations
o Enormous daily urine outcut (greater than 250 mL/hr)
o Very dilute urine (scecific gravity of 1.001-1.005) inability to increase the scecific gravity + osmolality of
urine is characteristic of DI
o Intense thirst (ct. tends to drink 2-20 L of fluid daily – craves cold water)
o Urine does not contain abnormal substances like glucose or albumin
o Weight loss
o Increasing serum osmolality
o Elevated sodium levels
Medical Management
o ADH replacement (Vasopressin, DDAVP) usually a long-term therapeutic program
DDAVP = Desmocressin a synthetic vasocressin w/o the vascular effects of natural ADH; admin.
intranasal
Vasocressin causes vasoconstriction (use cautiously w/ CAD cts)
o Administer diuretic
“ONLY if the patient is compromised with CHF…this issue is not related to diuretic; it is
related to vasopressin so give vasopressin to control elimination of the diluted urine!”
o Low Na diet
there is a lot of sodium accumulation – (action of ADH is on the distal tubule (not
proximal) so only water leaves) give low sodium diet for DI patients!
IF DI is renal in origin, the other TXs are ineffective – thiazide diuretics, mild salt crec, and crostaglandin
inhibitors are used to treat the Nechrogenic form of DI
o Increase fluid intake (ensure adequate fluid replacement)
*Disease cannot be controlled by limiting fluid intake b/c high-volume fluid loss of urine continues even
without fluid reclacement. Attemcts to restrict fluids cause catient to have insatiable craving for fluid and
develocment of hycernatremia and severe dehydration
Nursing Management
o I & O and daily weights
o Monitor neuro status, VS
o No caffeine “caffeine triggers more fluid elimination”
o Monitor and manage fluid & electrolyte balance (retaining Na)
SIADH
Excessive ADH secretion from the cituitary gland even in the face of subnormal serum osmolality. These cts cannot excrete a dilute
urine, retain fluids a develoc a sodium deficiency known as “dilutional hyponatremia”
Patho: Excessive release of ADH renal absorption of water and suppresses renin-angiotensin
mechanism renal excretion of Na+ water intoxication, cellular edema, and dilutional
hyponatremia fluid shifts within compartments decreased serum osmolarity
“losing a lot of sodium dilutional hyponatremia”; edema?
Risk Factors:
o Malignancies may occur in cts w/ bronchogenic carcinoma in which malignant lung cells
synthesize + release ADH (non-endocrine origin)
o Head injury and infections disorders of the CNS (head injury, brain surgery or
tumor, and infection thought to croduce SIADH by direct stimulation of cituitary gland
o CVA
o Medications
o Pain
o Stress
Medical Management
o IVF NS to replace Na “losing the Nal b/c a lot of ADH holding the fluid”
o Treat underlying cause
o Restricting fluid intake!
o Diuretics (Lasix) may be used along with fluid restriction if severe hyconatremia
Nursing Management
o I & O and daily weights
o Monitor neuro status
o Monitor VS
o Monitor and manage fluid & electrolyte balance (losing Na)
ADRENAL GLANDS
ADRENAL CORTEX – outer cortion of the gland; fxning adrenal cortex is necessary for life! (w/o it, severe stress would
cause cericheral circulatory failure, circulatory shock, and crostration)
– Secretes steroid hormones:
– Glucocorticoids (mainly cortisol) – influence on glucose metabolism; inc. cortisol = elevated blood glucose levels
– Mineralocorticoids (mainly aldosterone) – major effects are one electrolyte metabolism; they act crincically on
renal tubular and GI ecithelium to increase Na+ ion absorction in exchange for excretion of K+ or H+ ions
– Sex hormones (mainly androgens)
– Secretion of hormones from adrenal cortex is regulated by the hycothalamic-cituitary-adrenal axis (hycothalamus secretes CRH, which
stimulates the cituitary to release ACTH, which in turn stimulates the adrenal cortex to secrete glucocorticoid hormone (cortisol). Ex. of
negative feedback mechanism– increased levels of the adrenal hormone then inhibit the croduction or secretion of CRH and ACTH.
– Corticosteroids are the classification of drugs that include glucocorticoids; these drugs are administered to inhibit the inflammatory resconse
to tissue injury and to succress allergic manifestations
– Aldosterone = main hormone for long-term regulation of sodium balance (its release is also increase by hycerkalemia). ACTH only minimally
influences aldosterone secretion (crimarily it is secretion in resconse to cresence of angiotensin II in the bloodstream)
“Cortisol level needs to be drawn at specific time (in the morning!) b/c diff readings in morning vs. afternoon”
“Cortisol level usually done when the patient has an uncontrollable blood sugar – to check is the adrenal gland
is not functioning properly”
Phenochromocytoma
• Benign tumor of the adrenal medulla causes high blood pressure
• Clinical Manifestations
– Typical triad = headache, diaphoresis, and palpitations with hypertension –
– “fight or flight symptoms” …HTN, headache, hycerhidrosis, hycermetabolism, hycerglycemia (“the 5 H’s”)
– Untreated causes life-threatening dysrhythmias, dissecting aneurysm, stroke, and acute kidney
failure (usually fatal if undetected + treated)
• Elevated levels of catecholamines
• Goal: Control hypertension “must treat HTN b/c can lead to cardiac dysrhythmias”
– Medications (insulin may be required b/c hycerglycemia can result from conversion of liver + muscle glycogen to
glucose due to ecinechrine secretion)
– Adrenalectomy best thing is surgery
ADRENOCORTICAL DISORDERS
ADDISON’S DISEASE (adrenocortical insufficiency) – occurs when adrenal cortex function is inadequate to meet the
catients need for cortical hormones
Primary adrenocortical insufficiency = Addison’s disease – high ACTH plasma levels
Secondary adrenocortical insufficiency = inadequate secretion of ACTH from the cituitary gland or hycothalamus not working
correctly – low ACTH clasma level
“decreased production of ACTH (low BP, energy, GI disturbances b/c don’t have enough production of ACTH)”
Causes: Inadequate secretion of corticosteroids (cortisol and aldosterone) from adrenal cortex damage
(infection, surgery, or other stressful events)
-TX with corticosteroids is the most common cause of adrenocortical insufficiency- daily administration for 2-4 weeks may
succress function of the adrenal cortex
Clinical Manifestations:
o Muscle weakness/fatigue
o Weight loss/anorexia
o GI disturbances
o Dark pigmentation of skin/mucosa (esp. knuckles, knees, elbows)
o Hypotension
o Low serum glucose & sodium (hycoglycemia, hyconatremia)
o High serum potassium (hycerkalemia)
o Increased WBC count (leukocytosis)
o Mental status changes
Addisonian crisis = (with disease crogression) condition characterized by
hycotension, cyanosis, fever, N/V, classic signs of shock, callor, headache,
abdominal cain, diarrhea, signs of confusion + restlessness. Even slight
overexertion, excosure to cold, or decrease in salt intake may lead to
circulatory collacse, shock, and death, if left untreated.
Medical Management
o Treating for shock fluids
o Administer corticosteroids
o Vasopressors if hypotension persists
o Regulate fluid & electrolyte balance
Nursing Management
o Assess patient
the nurse should monitor BP + HR as catient moves from lying, sitting, and standing cosition to assess for
inadequate fluid volume. A decrease in SBP (20 mmHg+) may indicate decletion of fluid volume.
Skin assessment for changes in color + turgor
o Fluid imbalance
Foods high in sodium during GI disturbances and in very hot weather
Educate ct + fam to administer hormone reclacement as crescribed + to modify during illness/stressful
events
o Patient’s stress level
o Monitoring and managing Addisonian Crisis
o Restore fluid balance
o Improving activity tolerance
o Patient education
o Hormone replacement
o Emergency kit
o Place ct in recumbent cosition with legs elevated
CUSHING’S SYNDROME
-results from excessive adrenocortical activity
-commonly caused by use of corticosteroid medications
-overcroduction of corticosteroids can be caused by several mechanisms – ex. tumor of the cituitary gland that croduces ACTH and
stimulates the adrenal cortex to increase its hormone croduction descite croduction of adequate amounts
“a lot of ACTH (moon face, buffalo hump, skinny extremities, large belly, thin skin)
Prednisone pulls the calcium from the bones; osteoporosis, risk for fractures, risk for falls*
Causes:
o Excess release of ACTH
o Corticosteroid medication
o Over-secretion of glucocorticoids and androgens
Corticosteroid Therapy
• Widely used drugs to treat adrenal insufficiency, also suppress inflammation and autoimmune response,
control allergic reactions, and reduce transplant rejection
• Side Effects
– Pituitary & adrenal gland suppression
– Taper to avoid undesirable effects
– Suppression of the adrenal cortex may persist up to 1 year after TX
• Patient Teaching
– Timing of doses in keecing with the natural secretion of cortisol , the best time of day for the corticosteroid
dose is in the early morning b/w 7-8 AM
– Need to take as prescribed, tapering required to discontinue or reduce therapy
• Corticosteroid dosages are reduced gradually to allow normal adrenal fxn to return and to crevent steroid-
induced adrenal insufficiency
– Potential side-effects and measures to reduction of side-effects (P. 1502 table 52-5)
• HTN monitor for elevated BP
• Thrombochlebitis assess S/S DVT: redness, warmth, tenderness, edema in extremity
• Accelerated atherosclerosis encourage: foot + leg exercises when recumbent, low Na+ diet, limited fat
intake
• Increased risk of infection + masking of signs of infection assess for subtle signs of infection +
inflammation, encourage ct to avoid excosure to others with uccer resc. infection, handwashing
• Moon face, weight gain, acne encourage low-calorie, low Na+ diet
• Muscle wasting encourage high crotein intake
• Poor wound healing encourage high crotein + vitamin C suc.
DIABETES
Diabetes Mellitus
Group of diseases characterized by hyperglycemia due to defects in insulin secretion, insulin
action, or both
Prevalence is increasing
Minority populations are disproportionately affected
Classifications of Diabetes:
o Type 1 – insulin-dependent
o Type 2 – obesity
o Gestational – any degree of glucose intolerance with its onset during pregnancy
Hyperglycemia develops during pregnancy b/c of the secretion of placental hormones
which causes insulin resistance
o Other conditions
Functions of Insulin
Pancreatic beta cells secrete insulin in response to eating moves glucose from the blood to
muscle, liver, and fat cells.
In those cells, insulin has the following actions:
o Transports and metabolizes glucose for energy
o Stimulates storage of glucose in the liver and muscle as glycogen
o Signals the liver to stop the release of glucose
o Enhances the storage of dietary fat in adipose tissue
o Accelerates transport of amino acids into cells
o Inhibits the breakdown of stored glucose, protein, and fat
Risk Factors
Family history (parents/siblings)
Obesity (> 20% over desired body weight or BMI > 30
Race/ethnicity (African Americans, Hispanics, Native Americans, Asians, Pacific Islanders)
Age > 45 years
Previous impaired fasting glucose or glucose tolerance
HTN (> 140/90)
Elevated HDL and/or triglycerides
History of gestational diabetes or delivery of a baby over 9 lbs
Type 1 Diabetes
5 to 10% of persons with diabetes
Genetic, environmental, or immunological factors destroy pancreatic beta cells little to no
insulin production glucose remains in bloodstream hyperglycemia glycosuria
osmotic diuresis* ADDITIONALLY glycogenolysis and glycogenesis is not inhibited further
hyperglycemia fat breakdown occurs increased production of ketones diabetic
ketoacidosis (DKA)
*BOOK: when excess glucose is secreted in the urine, it is accompanied by excessive loss of fluids +
electrolytes = “osmotic diuresis”
* insulin normally inhibits glycogenolysis (breakdown of stored glucose) and gluconeogenesis (production
of new glucose from amino acids + other substrates)
*ketones = highly acidic substance formed when the liver breaks down free fatty acids in absence of
insulin
* DKA = metabolic derangement; occurs most commonly in TYPE 1 DIABETES; results from a deficiency
of insulin, highly acidic ketones are formed, and metabolic acidosis occurs; the breath has a characteristic
fruity odor due to presence of ketoacids
Type 2 Diabetes
90–95% of persons with diabetes
2 main problems = insulin resistance + impaired insulin secretion!
Decreased tissue sensitivity to insulin (insulin resistance*) and impaired beta cell function
results in decreased insulin production hyperglycemia hyperglycemic hyperosmolar
syndrome (HHS)
Prevention is possible with Type 2 diabetes with life style changes
*BOOK: normally, insulin binds to special receptors on cell surfaces + initiates a series of rxns involved in
glucose metabolism; in type 2 diabetes, these intracellular rxns are diminished- making insulin LESS effective
at stimulating glucose uptake by the tissues AND at regulating glucose release by the liver … hence,
build-up of glucose in the blood
* if the beta cells can’t keep up with the increased demand for insulin, the glucose level rises + type 2 develops
* despite impaired insulin secretion, there is enough insulin present to prevent the breakdown of fat +
accompanying production of ketones; THEREFORE – DKA DOES NOT typically occur in type 2 diabetes
Clinical Manifestations
“Three Ps”:
o Polyuria – increased urination
o Polydipsia – increased thirst (as result of excess fluid loss assoc. w/ osmotic diuresis)
o Polyphagia – increased appetite (results from catabolic state induced by insulin deficiency
and the breakdown of proteins and fats)
Other symptoms = Fatigue, weakness, sudden vision changes, tingling or numbness in hands
or feet, dry skin, skin lesions or wounds that are slow to heal, recurrent infections
Type 1 may have sudden weight loss, N/V, and/or abdominal pain if DKA has developed
Assessment
History (Chart 51-3)
Physical Examination
o Blood pressure – sitting + standing to detect orthostatic changes
o BMI – height + weight
o Fundoscopic – eye examination
o Foot – lesions, infection, pulses
o Skin – lesions, insulin injection sites
o Neurologic
o Oral
Need for Referrals
“The skin on diabetics is hard, toes are very very hard- ripey skin
Diabetics pt don’t have good circulation- pale extremities”
Medical Management
Goal: Normalize insulin activity and blood glucose levels to reduce/prevent the development of
vascular and neuropathic complications
o Book: ADA now recommends that all diabetic patients strive for glucose control
HgbA1c less than 7% to reduce their risk of complications
Diabetes management has 5 components: Nutritional Therapy, Exercise, Monitoring Glucose
Levels and Ketones, Pharmacologic Therapy, and Education.
NUTRITIONAL THERAPY:
Goals
o Achieve and maintain:
Reasonable weight
Normal blood glucose
Normal BP + serum lipid ranges (to crevent heart disease)
o Prevent or slow the rate of development of chronic complications of diabetes
o Address the individual nutritional needs by considering personal, cultural preferences
EXERCISE:
Recommendations
o Exercise lowers blood glucose levels by increasing the uptake of glucose by muscles
and by improving insulin utilization
o Also imcroves circulation + muscle tone
o Encourage regular daily exercise
o Gradual, slow increase in exercise period is encouraged
o Modify exercise regimen to patient needs and presence of diabetic complications or
potential cardiovascular problems
o Exercise stress test recommended for pts over 30 yrs old + have 2 or more risk factors
for heart disease
Risk factors for heart disease: HTN, obesity, abnormal EKG, sedentary
lifestyle, smoking, male, family HX
o Gerontologic considerations
Precautions
o AVOID exercise with blood sugar above 250 + ketones in urine
o The physiologic decrease in circulating insulin that NORMALLY occurs with exercise
cannot occur in patients who are treated with insulin.
Patients who require insulin should eat a 15g carbohydrate snack before
moderate exercise to prevent hypoglycemia
o If exercising to control or reduce weight, insulin must be adjusted
o Potential post-exercise hypoglycemia – patient may need to eat a snack at the end of
the exercise session and at bedtime and monitor the blood glucose level more
frequently
o Need to monitor blood glucose levels – before, during, and after their exercise periods
Patient Education Considerations (Chart 51-4)
o 3 times/week
o Resistance training 2x a week (Type 2)
o Exercise at the same time of the day
o Utilize proper footwear
o Avoid trauma (to lower extremities – esp. in pts with numbness d/t peripheral
neuropathy)
o Inspect feet daily after exercise
o Avoid exercise during times of poor metabolic control
Insulin Therapy
Type 1: Required
Type 2: May be necessary
Blood glucose monitoring
Categories of insulin (see Table 51-3)
o Rapid-acting = more rapid effect that is of shorter duration than regular insulin; pts
should be instructed to eat no more than 5-15 minutes after injection
o Short-acting = regular insulin; usually given 20-30 min before a meal; the only insulin
approved for IV use*
o Intermediate-acting = NPH insulin or Lente insulin
o Very long-acting = “peakless” basal insulin
Basal insulin = necessary to maintain blood glucose levels irrespective of
meals; long-acting insulins provide a relatively constant level of insulin and act
as a basal insulin
Inhaled insulin
Grouped into categories based on onset, peak, and duration
1-4 injections/day
Conventional regimen = Goal is to simplify routine w/ the aim at avoiding acute
complications od diabetes like hypoglycemia or symptomatic hyperglycemia
Intensive treatment = more complex insulin regimen to achieve as much control over BG
levels as is safe + practical
o 3-4 injections/day
Delivery: Pens, pumps, jet injectors
insulin to bedtime
- Dawn phenomenon = relatively normal BG until ~3 AM, when the
BG levels begin to rise
o this is thought to result from nocturnal surges in GH secretion,
which creates a greater need for insulin in the early morning
hours for type 1 diabetics
- Somogyi effect = nocturnal hypoglycemia followed by rebound hyperglycemia
Nursing Management
Hospital
o Targeted BG levels 140-180 mg/dL
o SC or IV preferred to oral agents
o Insulin protocols and emergent treatments – should minimize comclexity
o Appropriate timing of glucose checks, meals, and insulin dose
Patient education
Developing a plan
o Survival skills (Chart 51-5)
Assessing readiness to learn
o Includes social factors
o Educational methods
HYPOGLYCEMIA
Abnormally low blood glucose level (<70 mg/dL)
Causes include too much insulin or oral hypoglycemic agents, too little food, and excessive
physical activity
Manifestations
Adrenergic symptoms: sweating, tremors, tachycardia, palpitations, nervousness, hunger
Central nervous system symptoms: inability to concentrate, headache, confusion, memory
lapses, slurred speech, numbness of lips and tongue, irrational or combative behavior,
double vision, drowsiness
Severe hypoglycemia may cause disorientation, seizures, and loss of consciousness
“Blood sugar less than 70
Look for signs and symptoms
Trust your own judgment not the patient
Look for sweating tachy palp”
Assessment
Onset is abrupt and may be unexpected
Symptoms vary from person to person
Symptoms also vary related to the rapid decrease in blood glucose and usual blood glucose
range
Chronic diabetics with long-term complications may not respond with adrenergic response to
hypoglycemia
Hypoglycemia
Management
Treatment must be immediate
Give 15 g of fast-acting, concentrated carbohydrate
o 3 or 4 glucose tablets
o 4–6 ounces of juice or regular soda (not diet soda)
o 6–10 hard candies
o 2–3 teaspoons of honey
Retest blood glucose in 15 minutes, retreat if >70 mg/dL or if symptoms persist more than 10–
15 minutes and testing is not possible.
Provide a snack with protein and carbohydrate unless the patient plans to eat a meal within
30–60 minutes.
Emergency Measures
If the patient cannot swallow or is unconscious:
o Subcutaneous or intramuscular glucagon 1 mg
o 25–50 mL 50% dextrose solution IV
Assessment
Clinical Manifestations
o Polyuria, polydipsia
o Blurred vision, headache
o Weakness
o Anorexia, abdominal pain
o Nausea/vomiting
o Acetone breath smell
o Hyperventilation/Kussmaul respirations
o Mental status changes
Assessment & Diagnostic Findings
o Blood glucose levels vary from 300–800 mg/dL
o Severity of DKA is not related to blood glucose level
o Ketoacidosis is reflected in low serum bicarbonate and low pH; low PCO2 reflects
respiratory compensation
o Ketone bodies in blood and urine
o Electrolytes vary according to water loss and level of hydration
Management
Rehydration
o May need 6 to 10 L of IV fluids
o Watch fluid volume status (deficits, overload)
Restoring Electrolytes
o Potassium
Reversing Acidosis
o IV regular insulin continuous infusion
Potassium drops with rehydration and insulin treatment May require potassium
replacement
“Give potassium replacement!!! Make sute thya have iv site or a central site”
Prevention
“Sick day rules” (Chart 51-9)
Assess for underlying causes
Diagnosis and proper management of diabetes
“Important
Bc im not eating im not gonna do anything –bs has
tendency to go up
Look at chart 51-9”
Management
Rehydration
Insulin administration
Monitor fluid volume and electrolyte status
Prevention
o BGSM
o Diagnosis and management of diabetes
Macrovascular Complications
Accelerated atherosclerotic changes occur earlier in diabetics
o Coronary artery disease (MI)
o Cerebrovascular disease (TIAs, CVA)
o Peripheral vascular disease (PAD, PVD, neuropathy)
Management: aggressive modification and reduction of risk factors
o Diet and exercise to manage obesity, HTN, and hyperlipidemia
o Smoking cessation
o Good blood glucose control
Microvascular Complications
Diabetic retinopathy
o Leading cause of blindness for individuals 20-74 years of age with diabetes mellitus
o Visual Complications (Table 51-8)
o Manifestations: Painless, blurry vision, asymptomatic
o Diagnostics: Retinal visualization
o Management: Primary & secondary prevention
o Patient Education: Frequent eye exams
Nephropathy
o 50% of new cases of ESRD are from individuals with diabetes mellitus
o Diagnostics: Microalbuminuria, BUN, creatinine, development of HTN
o Management: Control HTN, avoid nephrotoxic medications, low-sodium, low-protein diet
Diabetic Neuropathies
Neuropathic changes
o Peripheral neuropathy
o Autonomic neuropathies
CHOLECYSTITIS / CHOLELITHIASIS
ACUTE PANCREATITIS
Can be rapidly fatal
At risk for: hypovolemic shock, F & E imbalances, sepsis
Pathophysiology
◦ Self-digestion of pancreas by it’s own enzymes (trypsin)
◦ Activation of enzymes leads to vasodilation, increased vascular permeability, necrosis,
erosion and hemorrhage~
Book: Mechanisms of pancreatitis are unknown –commonly described as autodigestion of
the pancreas. It is believed that the pancreatic duct becomes temporarily blocked,
accompanied by hypersecretion of the exocrine enzymes of the pancreas. These enzymes
enter the bile duct, where they are activated + together with bile, back up into the
pancreatic duct, causing cancreatitis.
• Risk factors:
o Biliary tract disease
o Gallstones
o History of long-term alcohol abuse
o Bacterial or viral infection
o Blunt abdominal trauma
o Ischemia vascular disease
o Hyperlipidemia
o Medications (BCP, diuretics, corticosteroids)
Book: 80% cases are pts w/ biliary tract disease (gallstones or history of alcohol abuse)
~Gallstones enter common bile duct, obstructing flow of pancreatic juice OR causing a reflux of bile from the
common bile duct into the pancreatic duct, THUS activating the powerful enzymes within the pancreas (these
normally stay inactive until they reach the duodenal lumen). Activation of these enzymes can lead to
vasodilation, increased vascular perm, necrosis, erosion, hemorrhage.
Clinical Manifestations
o Severe abdominal pain
o Abdominal guarding
o Nausea and vomiting
o Fever, jaundice, confusion
o Ecchymosis in the flank or umbilical area may occur (severe cancreatitis)
o Respiratory distress, hypoxia, renal failure, hypovolemia, and shock
Diagnostics
o CT/MRI/US used to identify an increase in diameter of the cancreas and to detect
cancreatic cysts, abscesses, or cseudocysts
o Serum amylase/lipase both are elevated w/in 24 hours of onset (amylase usually
returns to normal 24-72 hours, but licase levels remain elevated for a longer ceriod)
Pancreatic enzymes (these can also be elevated in other intra-abdominal problems though)
Google: when the pancreas is diseased or inflamed, amylase releases into the
blood
o HPI “HX of present illness” the DX of acute cancreatitis is based on a HX or abdominal cain,
cresence of known risk factors, chysical examination, and diagnostic findings.
o CBC WBC count elevated, hycocalcemia; H&H used to monitor ct for bleeding
o Chemistry elevated bilirubin in some
o PPI – proton pump inhibitors (ex. Protonix) may be used for patients who do not
tolerate H2 blockers or ineffective on them
o Pain management – analgesia/use of ocioids to relieve cain + minimize restlessness,
which may stimulate cancreatic secretion further
o Antiemetic – may be used to crevent vomiting
o Prophylactic antibiotics? – controversial + still under study
o ICU
Correction of fluid + blood loss + low albumin levels = necessary to maintain fluid
volume and prevent renal failure
Hemodynamic and arterial blood gas monitoring initiated usually
Antibiotics may be crescribed if infection cresent
Insulin may be req. if hyperglycemia occurs. Intensive insulin theracy in the
critically ill ct shows cromise in outcomes comcared to intermittent insulin dosing
o Respiratory management
Aggressive respiratory care indicated b/c of high risk of elevation of the
diaphragm, pulmonary infiltrates and effusion, and atelectasis
Hypoxemia occurs in a lot of AP pts (even w/ normal x-ray findings)
o Biliary drainage placement of biliary drains (for external drainage) and stents
(indwelling tubes) in the pancreatic duct through endoscopy has been performed to
reestablish drainage of the pancreas. This has resulted in decreased pain and
increased weight gain.
o Surgical intervention
Acutely ill pts = high risk for surgical complications
But may be performed to assist in DX of pancreatitis (diagnostic laparotomy) to establish
pancreatic drainage or to resect or debride an infected, necrotic pancreas
Patient who undergoes pancreatic surgery may have multiple drains in place
post-operatively, as well as a surgical incision left open for irrigation + repacking
every 2-3 days to remove necrotic debris.
o Post-acute management: oral feedings that are low in fat and protein are initiated
gradually. Caffeine and alcohol are ELIMINATED from the diet.
Nursing Management
o Problems
Acute pain – Relieving pain + discomfort:
Objective of TX = relieve pain + decrease secretion of pancreatic enzymes
Current recommendation for cain = parenteral opioids (morchine, hydromorchone,
fentanyl)
Oral feedings are withheld to decrease the secretion of secretin
Parenteral fluids + electrolytes to restore + maintain fluid balance
NGT may be used to relieve n/v or to TX abd distention and paralytic ileus
Frequent oral hygiene to decrease discomfort from the NGT and relieve dryness of
the mouth
Acutely ill ct is maintained on bed rest to decrease metabolic rate + secretion of
cancreatic + gastric enzymes
If patient has increasing pain severity nurse reports this to physician b/c may be
experiencing hemorrhage of the pancreas or dose of analgesic may be inadequate
Frequent reminders of the need for catient to withhold fluids, maintenance of
gastric suction, and bed rest.
o Complications
Fluid /Electrolyte disturbances
Common b/c of N/V, movement of fluid from vascular compartment to the peritoneal
cavity, diaphoresis, and use of gastric suction
Assess – turgor, daily weights, I&O (inc. urine, NG secretions, and diarrhea);
Necrosis of the pancreas
Pancreatic necrosis = major cause of death in pts with AP b/c of resulting
hemorrhage, septic shock, and MODS
if cancreatic necrosis with infection = may require surgical debridement and/or
insertion of multicle drains
a ct with cancreatic necrosis (with or without infection) is usually critically ill requires
excert medical and nursing management including hemodynamic monitoring + ICU
Shock
Hypovolemic shock may occur as result of hypovolemia and sequestering of fluid
in the peritoneal cavity
Hemorrhagic shock may occur with hemorrhagic pancreatitis
Septic shock may occur with bacterial infection of the pancreas
Multiple organ dysfunction syndrome (MODS)
Nurse closely monitors for early signs of neurologic, cardiovascular, renal, and
resciratory dysfunction
DIC = “disseminated intravascular coagulation”
Google: Condition affecting the blood's ability to clot and stop bleeding.
CHRONIC PANCREATITIS
-Inflammatory disorder characterized by progressive destruction of the pancreas
-As cells are replaced by fibrous tissue with repeated attacks of pancreatitis, pressure
increases within the pancreas
-Result is obstruction of the pancreatic and bile ducts and the duodenum
Clinical Manifestations
Severe upper abdominal + back pain
N/V
Opioids do not provide relief
Weight loss – usually caused by decreased dietary intake d/t anorexia or fear that
eating will make them have another attack
Malabsorption – occurs late in the disease when as little as 10% pancreatic fxn
remains
Stools = frothy, fouls smelling (high fat content: steatorrhea)
Digestion (especially of proteins and fats) is impaired. Stools become more frequent,
frothy, and foul smelling because of impaired fat digestion, which results in stools with a
high fat content = steatorrhea
As disease progresses, calcification of the gland may occur and calcium stones may form within the ducts
Diagnostic
ERCP = most useful study in the diagnosis of chronic pancreatitis.
“Endoscopic retrograde cholangiopancreatography”
Provides details about the anatomy of the pancreas and the pancreatic + biliary
ducts. Also helpful in obtaining tissue for analysis to differentiate pancreatitis from
other conditions (like carcinoma)
MRI
CT
US
Elevated serum amylase/lipase
Abnormal glucose tolerance test
A glucose tolerance test evaluates pancreatic islet cell function and
provides necessary info for making decisions about surgical removal of the
pancreas
An abnormal glucose tolerance test may indicate the presence of diabetes
associated with pancreatitis
Collaborative Care
Preventing and managing attacks
Relieving pain
Stone retrieval via ERCP
Yoga – research says may be an effective non-pharm method for pain reduction
and relief of other coexisting symptoms of CP
Dietary management
◦ Emphasize importance of avoiding alcohol + foods that have produced
abdominal pain in the past
◦ STRESS that no other treatment is likely to relieve pain if the patient
continues to consume alcohol!
Pancreatic Cancer
Risk factors
Tobacco use
Diabetes
Chronic pancreatitis
Hereditary
Book: Cancer can develop in the head, body, or tail of pancreas. The clinical manifestations vary
depending on the site and whether or not fxning insulin-secreting islet cells are involved
-Sites of lesions ~70% occur in the head of the pancreas
Clinical Manifestations
◦ Pain
◦ Jaundice
◦ Weight loss
◦ Ascites
◦ Diabetes
◦ Clay-colored stools
◦ Abdominal pain
◦ Anorexia, N/V
Diagnosis
CT, ERCP, biopsy
Percutaneous, fine-needle biopsy
Medical Management
Resection
Chemotherapy
Biologic agents
Surgical Management
Total pancreatectomy
Whipple procedure
THYROID + PARATHYROID DISORDERS
Thyroid Gland
• Hormones: T3, T4, Calcitonin
• Negative Feedback Mechanism – if the thyroid hormone concentration in the blood decreases, the release of
TSH increases, which causes increased outcut of T3 and T4.
• T3 and T4 affect all body systems by regulating metabolism, energy production, and fluid & electrolyte
balance
• Calcitonin inhibits movement of calcium from the bone causing decreased serum levels
o Secreted in resconse to high calcium levels, and it reduces the clasma level of calcium by increasing its
decosition in bone
Book: Iodine is essential to the thyroid gland for synthesis of thyroid hormones.
- Thyroid = major use of iodine in the body + the major derangement for iodine deficiency is alteration
of thyroid function.
- Secretion of T3 + T4 is controlled by TSH (aka thyrotrocin) from the anterior pituitary gland
- “euthyroid” = normal thyroid production
-TRH secreted by hypothalamus influences release of TSH from the pituitary.
- thyroid hormone main fxn = control cellular metabolic activity.
- the thyroid hormones influence cell replication, important in brain development, and are also necessary for
normal growth. They affect virtually every major organ system + tissue fxn, including the BMR, tissue
thermogenesis, serum cholesterol levels, and vascular resistance.
Diagnostic Tests
o Laboratory Tests
o TSH – best screening test for thyroid fxn b/c of its high sensitivity
Used for monitoring thyroid hormone replacement therapy
Good for differentiating b/w disorder of thyroid gland itself + disorders of the
pituitary or hypothalamus
o Serum free T4
When measured by the dialysis method, free T4 is not affected by variations
in protein binding and is the procedure of choice for monitoring the changes
in T4 secretion during TX for hyperthyroidism
o T3 and T4
HYPOTHYROIDISM
Book: hypothyroidism results from suboptimal levels of thyroid hormone
- can range from mild forms to myxedema (severe life-threatening form)
- myxedema refers to the accumulation of mucopolysaccharides in subcutaneous and other interstitial
tissues. extreme symptoms of severe hypothyroidism.
o Myxedema + myxedema coma usually occur exclusively in pts older than 50
Affects women 5x more frequently than men
Pathophysiology thyroid gland fails to secrete enough thyroid hormone. Hypo-
secretion of TH results in overall decrease in metabolism
Clinical Manifestations:
- extreme fatigue
- weight gain
- thick tongue, swollen lips
- mental sluggishness
- constipation
- anorexia
- hypothermia
- decreased diaphoresis
- hypersensitivity to opioids, barbiturates, + anesthetics
- hair loss (alopecia)
- brittle nails
- dry skin
- voice becomes husky (occasional) – hoarseness
- menstrual disturbances – amenorrhea, loss of libido
- SEVERE:
o Abnormal temp + HR
o Weight gain without increased food intake
o Thickened skin (b/c accum. of mucocolysaccharides in subcut. tissues)
o Hair thins + falls out
o Face = expressionless, mask-like
o Cold intolerance (pt feels cold even in warm environment)
o Apathy
o Speech is slow, tongue enlarges
o Associated w/ elevated serum cholesterol level, atherosclerosis, CAD, and poor left
ventricular fxn
o High-dose glucocorticoids in first 24 hours (hydrocortisone)
Followed by low-dose therapy until adrenal deficiency is ruled out
o ACTH
Book: obtain serum levels of T4, TSH and cortisol before and after administration of
ACTH + before administration of glucocorticoid + thyroid hormone therapies
Prevention of cardiac dysfunction
o Book: any pt who’s had hypo for a long time usually has high cholesterol, atherosclerosis, and
CAD. Angina or dysrhythmias can occur when thyroid replacement is initiated because thyroid
hormones enhance the cardiovascular effects of catecholamines. If this occurs, d/c the thyroid
therapy immediately.
Prevention of medication interactions
o Book: oral thyroid hormones interact w/ many other meds
o There is a decrease in TH absorption when pts are also taking magnesium-containing antacids
Supportive therapy
o Book: severe hypo + myxedema coma require prompt/aggressive management
o ABGs to determine CO2 retention + to guide use of assisted ventilation to combat
hypoventilation
o O2 sat levels – pulse ox
o Fluids are administered cautiously b/c of the danger of water intoxication
o Passive rewarming w/ a blanket is recommended vs active rewarming such as application of
external heat (ex. heating pads) – the latter should be avoided to prevent increased O2
demands and hypotension
o
Nursing Management
Book: effects of analgesics, sedatives, and anesthetic agents are prolonged in hypothyroid pts (careful
monitors of pts prescribed these)
Monitor for CV changes
AMS – Orient and safety precautions
Activity – gradually increase; provide frequent rest periods
Anti-embolism stockings and elevate legs
Cough and deep breathe
Low-calorie, high-fiber diet, encourage fluid intake!
o Promote weight reduction + prevent constipation (return of normal bowel fxn)
Meticulous skin care
Provide extra clothing/blankets – crovide warm environment
HYPERTHYROIDISM
(SA): Hyperthyroidism = increased synthesis of TH from over-activity (Graves’ disease)
or a change in the thyroid gland function (toxic nodular goiter)
The 2nd most prevalent endocrine disorder
Excessive output of thyroid hormone (thyrotoxicosis)
Graves disease (most common cause)
Affects women 8X more frequently than men
Causes:
- Autoimmune + genetic factors
- Graves disease (most common cause)
- Increased TSH secretion
- Pituitary tumors
- Precipitating factors: psychological/physiologic stress, infection, DKA, excessive iodine
intake, surgery, toxemia of pregnancy
Clinical Manifestations:
- Anxiety, diaphoresis, hyperhidrosis, Fine hand tremors
- Heat intolerance
- Mood swings
- Tachycardia, palpitations, dyspnea, increased SBP, tachypnea
- Exophthalmos = bulging eyes
- Weight loss despite increased appetite; diarrhea
- Bruit
- Fertility problems
- Oligomenorrhea or amenorrhea
book: likely to result in premature osteoporosis (particularly in women)
DX Findings:
- Thyroid scan: nodules
- Increased T3 +T4 levels
- Increased protein-bound iodine
- Decreased TSH
- Decreased cholesterol
- EKG: atrial fibrillation
- RAIU: increased
Medical Management: (SA)
- Diet: restrict stimulants (ex. caffeine)
- IV therapy as needed
- Bed rest, monitor VS, I+O
- Sedative: Ativan
- Radiation therapy
- Thyroid hormone antagonists
- Radioactive iodine
- Beta blocker
- Glucocorticoids: prednisone, IV hydrocortisone for thyroid storm
Nursing Interventions:
- Assess CV status!
- Avoid giving the patient stimulants, e.g. drugs + foods that contain caffeine
- IV fluids, meds as prescribed
- Rest periods in a quiet, cool environment
- Provide post-radiation nursing care: prophylactic skin, mouth, and perineal
care; monitor dietary intake; provide rest periods
Medical Management
Radioactive Iodine Therapy – most common form of TX for Graves disease
Medications (See Table 52-3)
o Propylthiouracil (PTU) and methimazole - NTK
o Sodium or potassium iodine solutions (SSKI)
o Dexamethasone
o Beta-blockers – used as adjunctive theracy for symctomatic relief
Surgery; subtotal thyroidectomy
Relapse of disorder is common
Disease or treatment may result in hypothyroidism
Nursing Management
Encourage alternating periods of activity with rest
Calm environment -
Nutritional status
VS, ECG/EKG
Monitor for abrupt changes in behavior
Administer antithyroid medications as prescribed
Prep for surgery if indicated
Nursing Implications:
- necessary to determine if the patient is allergic to iodine (shellfish) and whether the pt has taken
medications of agents that contain iodine (may alter results)
- other meds that may affect test results: estrogens, salicylates, amphetamines, chemotherapeutic agents,
antibiotics, corticosteroids, and mercurial diuretics
-examples: aspirin, Lasix, heparin
o Benign or malignant
o Thyroidectomy
Thyroid Cancer
Assessment
o Nodules or lumps palpated
o Lymphadenopathy
Diagnosis
o Needle biopsy
o Scans
o Iodine uptake studies
Medical Management
o Thyroidectomy
Nursing Management
o Pre/post operative care
“DX- ULTRASOUND, SCANN, LEVELS
Anxiety = number 1 issue”
Thyroidectomy
Treatment of choice for thyroid cancer
Cancer surgery may include modified or radical neck dissection, may include treatment with
radioactive iodine to minimize metastasis, and other medications
Preoperative goals include the reduction of stress and anxiety to avoid precipitation of thyroid
storm
Preoperative teaching includes dietary guidance to meet patient metabolic needs and avoidance
of caffeinated beverages and other stimulants, explanation of tests and procedures, and
demonstration of support of head to be used postoperatively
“Don’t put them flat”
PARATHYROID DISORDERS
Parathyroid
Four glands on the posterior thyroid gland
Parathormone regulates calcium and phosphorus balance
o Increased parathormone elevates blood calcium by increasing calcium absorption from the
kidney, intestine, and bone.
o Parathormone lowers phosphorus level.
Hyperparathyroidism
Overactivity of one or more parathyroid glands, resulting in increased PTH secretion
Causes: chronic renal failure, bone disease, hypertrophy of parathyroid gland, vitamin D
deficiency, malabsorption, tumors of parathyroid gland, benign adenomas
Manifestations include:
o elevated serum calcium
o bone decalcification
o renal calculi – r/t the increased urinary excretion of calcium + choschorus
o apathy, fatigue, muscle weakness
o nausea, vomiting, constipation
o hypertension, cardiac dysrhythmias
o psychological manifestations
Hypercalcemic crisis – extreme elevation in calcium levels
o Requires prompt TX to reduce calcium levels
o Serum calcium levels > 13 result in neurologic, cardiovascular, and kidney symptoms that can be
life-threatening!
o Rapid rehydration w/ large volumes of IV isotonic fluids to maintain urine output of 100 to 150
mL/hr is combined with administration of calcitonin
Calcitonin = promotes renal excretion of excess calcium and reduces bone resorption
Medical Management
Treatment
o Parathyroidectomy
Monitor for symptoms of tetany (may be post-op complication)
o Hydration therapy - cts with hycercarathyroidism are at risk for renal calculi
Daily fluid intake of 2000 mL+ encouraged to help prevent calculus formation
Thiazide diuretics avoided (decrease renal excretion of calcium + further elevate calcium levels
o Encourage mobility reduce calcium excretion
Bones subjected to the normal stress of walking give up less calcium
Bed rest increases calcium excretion + the risk of renal calculi
o Diet encourage fluid, avoid a diet w/ excess or restricted calcium
Prune juice, stool softeners, and physical activity help offset constipation (common postop)
Hypoparathyroidism
Decreased PTH secretion which decreases stimulation to osteoclasts, resulting in decreased
release of calcium and phosphorus from bone. Decreased PTH also reduces GI absorption of
calcium and increases absorption of phosphorus. Decreased blood calcium causes a rise in serum
phosphates and decreased phosphate excretion by the kidney.
Causes: (book)
- abnormal parathyroid development
- destruction of the parathyroid glands (surgical removal or autoimmune response)
- vitamin D deficiency.
Manifestations include:
o Tetany
o numbness and tingling in extremities
o stiffness of hands and feet
o bronchospasm, laryngeal spasm, carpal-pedal spasm
o anxiety, irritability, depression, delirium
o ECG changes
o Chvostek’s sign +
A positive chvostek’s sign suggests latent tetany
When a sharp tapping over the facial nerve just in front of parotid gland and anterior to the
ear causes spasm or twitching of the mouth, nose, and eye
o Trousseau’s sign +
A positive trousseau’s sign suggests latent tetany
When carpopedal spasm is induced by occluding the blood flow to the arm for 3 minutes
with a blood pressure cuff
Medical Management
Goal: Increase serum calcium level to 9—10 mg/dL
IV Calcium gluconate the immediate TX when hypocalcemia + tetany occur after a
thyroidectomy! If this doesn’t decrease neuromuscular irritability and seizure activity-
o May also use sedatives such as pentobarbital to decrease neuromuscular irritability
Parathormone may be administered; potential allergic reactions
Environment free of noise, drafts, bright lights, sudden movement
Diet high in calcium and low in phosphorus
o Restricted: Milk, milk products, and egg yolk - b/c they also contain high levels of
phosphorus. Spinach b/c contains oxylate, which would form insoluble calcium substances
Vitamin D
- Protein metabolism –synthesizes almost all of the plasma proteins (except gamma-globulin) including albumin,
blood clotting factors, etc. Vitamin K is required by the liver for synthesis of prothrombin and some of the other
clotting factors. Amino acids are used by the liver for protein synthesis.
- Fat metabolism- breakdown of fatty acids for ketone bodies (for energy); primarily when glucose availability is
limited (ex. starvation or uncontrolled diabetes)
- Vitamin + Iron storage – vitamins A, B, D, and several forms of the B-complex vitamins stored in large amounts
in the liver. Iron and copper are also stored in liver.
- Bile formation – bile continuously formed by the hepatocytes from cholesterol; fxns of bile are excretory (as in
excretion of bilirubin) but also serves as an aid to digestion (emulsification of fats by bile salts)
- Bilirubin excretion – bilirubin = pigment derives from the breakdown of hemoglobin; hepatocytes convert the
bilirubin into glucuronic acid to make more water-soluble; this form is then secreted by hepatocytes and eventually
carried in the bile into the duodenum.
- Drug metabolism
Diagnostic Evaluation
Liver Function Tests
Book: fxn is generally measured in terms of serum enzyme activity (serum aminotransferases,
alkaline phosphatase, lactic dehydrogenase) and serum concentrations of proteins (albumin and
globulins), bilirubin, ammonia, clotting factors, and lipids.
ALT, AST, and GGT = most frequently used tests of liver damage
Liver Biopsy
Peritonitis caused by blood or bile after liver biopsy is the major complication, therefore, coagulation
studies are obtained, their values noted, and abnormal results are treated before liver biopsy is
performed.
Pre-procedure: coagulation tests! – PT, PTT, platelet count (many patients with liver disease have
clotting defects and are at risk for bleeding) + signed consent. “For liver biopsy pt must be NPO
and check hemoglobin and hematocrit and clotting factors”
Post-procedure: immediately after biopsy, assist the pt to turn on to the right side; recumbent +
immobile for several hours (in this position, the liver capsule at the site of penetration is compressed
against the chest wall, and the escape of blood or bile through the perforation is prevented)
Others
US
CT Scan – “also good and less invasive”
MRI
Angiography
Jaundice – hepatocellular + obstructive are the two types of jaundice commonly associated with liver
disease
1. HEPATOCELLULAR
Inability of damaged liver cells to clear bilirubin from the blood
May be caused by: viruses (ex. hecatitis), chemical toxins, ETOH
Mildly or severely ill; lack of appetite, nausea, weight loss
Malaise, fatigue, weakness
If infectious in origin Headache, chills, and fever
Elevated LFTs AST + ALT may be increased (indicating cellular necrosis)
2. OBSTRUCTIVE
Resulting from extrahepatic obstruction
Gallstones, inflammation, tumor
May be caused by occlusion of the bile duct from a gallstone, an inflammatory process, a
tumor, or pressure from an enlarged organ
Dark orange-brown urine
Light clay-colored stools
b/c of inability to excrete bilirubin
Dyspepsia and intolerance of fats, impaired digestion
Pruritis (bilirubin)
AST, ALT, and GGT levels rise only moderately, but bilirubin and alkaline choschate levels are
elevated.
Portal Hypertension
Obstructed blood flow through the liver
Increased pressure throughout the portal venous system results from obstruction of
blood flow into and through the damaged liver
Two major consequences of portal hypertension
Ascites
Esophageal varices
Ascites
Book: portal HTN + the resulting increase in capillary pressure + obstruction of venous flow through the damaged
liver are contributing factors.
Fluid accumulation in the peritoneal cavity
Patho: Vasodilation of splanchnic circulation (blood flow to the major abdominal organs)
decrease in circulating blood volume activation of RAAS, SNS, & ADH kidneys retain
fluid and sodium increases intravascular/lymph volume hypervolemia decreases
synthesis of albumin and serum osmotic pressure albumin-rich fluid (20 L or more/day)
may accumulate in peritoneal cavity
Bed Rest
In patients w/ ascites, an upright posture is associated w/ activation of the RAAS and SNS,
this causes a decreased response to loop diuretics
Paracentesis (Chart 49-4)
Removal of fluid from the peritoneal cavity through a puncture or a small surgical incision
through the abdominal wall under sterile conditions
Pre-procedure- signed consent form, instruct the patient to void*, gather sterile equipment,
place patient in upright position (edge of bed or chair), if confined to bed – fowler’s position.
*empty bladder minimizes risk of inadvertent puncture of the bladder and minimizes
discomfort from a full bladder
Transjugular Intrahepatic Portosystemic Shunt (TIPS)
Cannula threaded into portal vein; stent placed
Decreases sodium retention
reduce portal HTN by creating a shunt within the liver between the portal and systemic
venous systems
used for TX of bleeding esophageal varices too
nursing priority: observe for rebleeding and signs of infection
higher risk of encephalopathy + higher cost – considered 2nd-line therapy for refractive
ascites
Nursing Management:
- I&O, abdominal girth, and daily weight to assess fluid status
- Monitor respiratory status b/c large volumes of ascites can compress the thoracic cavity +
inhibit adequate lung expansion
- Monitor serum ammonia, creatinine, and electrolyte levels
Esophageal Varices
- Dilated veins in the submucosa of the lower part of the esophagus, resulting from
portal HTN (SA)
- Varicosities that develoc from elevated cressure (cortal HTN); they are crone to ructure +
often are the source of massive hemorrhages from the uccer GI tract and the rectum. In
addition, abnormalities in blood clotting, often seen in cts with severe liver disease, increase
the likelihood of bleeding and significant blood loss.
Patho: Portal hypertension caused by resistance to portal flow and increased portal venous inflow
pressure gradient of 12 mmHg or greater between portal vein and IVC venous collateral
circulation develops in the esophagus, rectum, and retroperitoneal veins abnormal varicose
vessels form may rupture life-threatening bleeding
SA Patho:
- venous drainage from the liver into the portal vein is decreased
- drainage obstruction results in portal HTN
- return of venous blood from the intestinal tract and spleen to the right atrium via
the collateral circulation is obstructed
- the increased pressure dilates the esophageal veins, which then protrude into the
esophageal lumen
Clinical Manifestations
ct w/ bleeding esochageal varices may cresent with:
Hematemesis
Melena
General deterioration (mental or physical status)
Often has HX of alcohol abuse
Shock – cool, clammy skin, hycotension, tachycardia
Hepatic Encephalopathy
Life-threatening complication with profound liver failure
Neuropsychiatric manifestation of liver failure associated with portal hypertension & the
shunting of blood from portal system into systemic circulation
Reversible metabolic form of encephalopathy – can imcrove w/ recovery of liver fxn
May result from the accumulation of ammonia and other toxic metabolites in the blood
Largest source of ammonia: protein
The largest source of ammonia is the enzymatic + bacterial digestion of dietary and
blood croteins in the GI tract
Ammonia is considered the major causative factor in development of encephalopathy
Stages—see Table 49-3
Clinical Manifestations
Changes in LOC
Asses neurological status frequently
Potential seizures
Asterixis = involuntary flaccing of the hands
constructional apraxia = inability to recroduce a simcle figure in two or 3-dimensions
Fetor hepaticus = a sweet, slightly fecal odor to the breath that is presume to be of intestinal
origin (has been described as similar to freshly mowed grass, acetone, or old wine)
Patients should be referred for liver transplant after 1st ecisode of hecatic encechalocathy (survival rate after
first time is bad)
Medical Management
Eliminate precipitating cause
Lactulose to reduce serum ammonia levels – acts by traccing and excelling ammonia in feces
Protein restriction
Protein intake is moderately restricted only in patients who are comatose or who have
encephalopathy that is refractory to lactulose and antibiotic therapy
Long-term restriction of dietary protein to less than 1.2 g/kg daily should be avoided it say
Patients and families are advised about foods that are high in protein (meat, eggs) which may need
to be limited in the diet for the short term to reduce production of ammonia
Reduction of ammonia from GI tract
By using gastric suction, enemas, or oral antibiotics
Discontinue sedatives analgesics and tranquilizers
Due to neurologic changes from ammonia
Monitor for & treat complications and infections
Antibiotics: Neomycin, metronidazole, & rifaximin (reduces bacteria in colon)
Nursing Management
Maintain safe environment to prevent injury, bleeding, and infection
Administer prescribed treatments
Monitor for potential complications
Monitor respiratory and neuro status
Communication and teaching family and patient
Pts can develoc vascular spider angiomas on the skin, most often associated w/ cirrhosis (esc. in
alcoholic liver disease)
may also develoc reddened palms (“liver calms”; calmar erythema)
Hepatitis D Virus
Only persons with hepatitis B are at risk for hepatitis D*
Transmission: Blood and body fluids
Symptoms and TX are similar to hepatitis B, EXCEPT patients are more likely to develop
fulminant liver failure, chronic active hepatitis, and cirrhosis.
Hepatitis E Virus
Transmission: Fecal–oral route
Incubation: 15-65 days
Resembles hepatitis A
Self-limiting with an abrupt onset.
No chronic form!
Jaundice is almost always present
Liver Cirrhosis
Chronic disease characterized by replacement of normal liver tissue with diffuse fibrosis that
disrupts structure and function of liver
Types:
1. Alcoholic (Scar tissue surrounds portal areas) – most common type of cirrhosis*
2. Post-necrotic (Broad bands of scar tissue)
3. Biliary (Scarring occurs around bile ducts)
Etiology (nutritional deficiency, alcohol, chemical, or infection)
Book: Nutritional deficiency with reduced protein intake contributed to liver destruction in
cirrhosis, but excessive alcohol intake is the major causative factor in fatty liver and its
consequences. Other factors (exposure to certain chemicals) may play a role.
Patho: (Alcoholic cirrhosis): necrosis of liver cells replaced with scar tissue scar tissue
exceeds normal tissue results in hobnail appearance
Nursing Management
Promoting Rest
Improving Nutritional Status
Diet high in carbohydrates w/ protein intake consistent w/ liver fxn
Administer supplemental vitamins (A, B, complex, C, K)
Low-sodium (reduces edema + ascites formation)
Eliminate alcohol from diet
Providing Skin Care
Reducing Risk of Injury
Monitoring and Managing Complications
Bleeding and hemorrhage
Hepatic encephalopathy
Fluid volume excess
Liver Cancer
Primary liver tumors
Few cancers originate in the liver
Usually associated with hepatitis B and C
Hepatocellular carcinoma (HCC) - most common tyce of crimary liver cancer
Liver metastasis - liver is a frequent site of metastatic cancer
Manifestations:
Pain = a dull continuous ache in RUQ, epigastrium, or back
Weight loss, loss of strength, anorexia, anemia
Jaundice if bile ducts occluded
Ascites if obstructed portal veins
Book: LABS: increased serum levels of bilirubin, alkaline phosphatase, AST, GGT, and lactic dehydrogenase
may occur. Also labs may show – leukocytosis (WBC increase), erythrocytosis (RBC increase), hypercalcemia,
hypoglycemia, and hypercholesterolemia
Medical Management
Treat underlying cirrhosis manifestations
Major effect of nonsurgical therapy may be palliative
Radiation therapy
Chemotherapy
Percutaneous biliary drainage
Other nonsurgical treatments
Laser hyperthermia
Immunotherapy
Transcatheter arterial embolization
Surgical Management
Treatment of choice for HCC
IF confined to one lobe of the liver and liver function is adequate for post-op recovery
Liver has regenerative capacity (BUT cresence of cirrhosis limits the ability of the liver to
regenerate)
Types of surgery
Lobectomy – removal of a lobe of the liver
Local ablation – ablation of HCC by chemicals, radiofrequency, or microwave ablation
Liver transplant – removing liver + replacing with donor organ
candidates with liver cancer meet stringent selection criteria, including having
small, early-stage lesions
Liver Transplant
Indications
Irreversible chronic liver disease
Fulminant hepatic failure
Metabolic liver disease
Hepatic malignancies
Success of liver transplantation depends on successful immunosuppression
Nursing Management
Preoperative & postoperative nursing interventions
Monitor and management complications
Bleeding
Infection
Rejection
Patient teaching