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Med Surg Exam 1

NUR 440
Exam I Blueprint
50 multiple choice questions, 3 select all that apply. You are allowed 70 minutes for Exam 1.
FIRST QUESTION OF THE EXAM: Adolescent with long history of Diabetes Mellitus, confused, flushed, acetone breath….
DKA was suspected, what type of insulin should be administered? …… Regular insulin
Diabetes Mellitus (Chapter 48)
Oral medications including Biguanides
● Oral Agents
○ Work on 3 defects of type 2 DM
■ Insulin resistance
■ Decreased insulin production
■ Increased hepatic glucose production
○ Can be used in combination
● Biguanides
● Metformin (Glucophage)
○ Reduces glucose production by the liver
○ Enhances insulin sensitivity at the tissue level and improves glucose transport into the cells
○ Beneficial effects on plasma lipids → may cause moderate weight loss
■ So useful in patients with type 2 DM and prediabetes who are overweight
○ Used in prevention of type 2 DM in those with prediabetes who are <60 and have risk factors such as
HTN or hx or gestational DM
○ **first chioce drug used in prevenetion of type 2 diabetes
○ Withhold if patient is undergoing surgery or radiologic procedure with contrast medium
■ Day or two before and at least 48 hours after
■ Monitor serum creatinine
○ Contraindications
■ Renal, liver, cardiac disease
■ Excessive alcohol intake
Increased insulin production from pancreas
Major side effect:hypoglycemia
- Glipizide (Glucotrol)
- Glyburide (Glynase)
- Glimepiride (Amaryl)
Increased insulin production from pancreas
Rapid onset: decrease hypoglycemia
Taken 30 minutes to just before each meal
Should not be taken if meal skipped
- Repaglinide (Prandin)
- Nateglinide (Starlix)
Alpha-glucosidase inhibitors
“Starch blockers” /;
- Slow down absorption of carbohydrate in small intestine
- Take with first bite of each meal
- Effectiveness is measured by checking 2 hour postprandial glucose levels
- Example:
- Acarbose (Precose)
- Miglitol (Glyset)
“Insulin sensitizers”
Most effective in those with insulin resistance
Improve insulin sensitivity, transport, and utilization at target tissues
- Pioglitazone (Actos)
- Rosiglitazone (Avianda)
Rarely used because of adverse effects
Dipeptidyl Peptidase- 4 (DDP-4) Inhibitor
Blocks inactivation of incretin hormones
- Increased insulin release
- Decreased glucagon secretion
- Decreased hepatic glucose production
Examples (gliptins)
- Sitagliptin (Januvia)
- Saxagliptin (Onglyza)
- Linagliptin (Tradjenta)
Sodium- Glucose Co- Transporter 2 (SGLT2) Inhibitors
SGLT2 inhibitors work by
- Blocking reabsorption of glucose by kidney
- Increasing glucose excretion
- Lowering blood glucose levels
- Canagliflozin (Invokana)
- Dapagliflozin (Farxiga)
- Empagliflozin (Jardiance)
Dopamine Receptor Agonist
Bromocriptine (Cycloset)
Mechanism of action unknown
Thought that patients with type 2 DM have low levels of dopamine
Increases dopamine receptor activity
Alone or in combination
Glucagon-like Peptide-1 Receptor Agonists
Stimulate glucagon-like peptide- 1 (GLP-1)
- Increase insulin synthesis and release
- Inhibit glucagon secretion
Slow gastric emptying
Increases satiety
Combination oral therapy
Blend two different classes of medications to treat diabetes
Improves adherence because patient takes fewer pills
Insulin types, onset, peak, duration
Nutritional therapy goals
Nutritional Therapy:
- Counseling
- Education
- Ongoing monitoring
- Interprofessional team
- Registered dietitian with expertise in diabetes management
Nutritional Therapy Goals:
- ADA healthy food choices
- Maintain blood glucose levels to as close to normal as safely possible
- Normal lipid profiles
- Blood pressure
- Prevent or slow complications
- Individual needs; personal, cultural preferences
- Maintain pleasure of eating
Nutritional Therapy: Type I DM
- Meal planning
- Based on usual food intake and preferences
- Balanced with insulin and exercise patterns
Day-to-day consistency makes it easier to manage blood glucose levels
More flexibility with rapid-acting insulin, multiple daily injections, and insulin pump
Nutritional Teaching: Type 2 DM
- Food composition
- Carbohydrates
- Fats
- Protein
- Alcohol
Administration of insulin
Administration of insulin:
- Absorption is fastest from abdomen, followed by arm, thigh, and buttock
- Abdomen is often preferred site
- Do not inject in site to be exercised
- Rotate injections within and between sites
Storage of insulin:
- Do not heat/freeze
- In use vials may be left at room temperature up to 4 weeks
- Extra insulin should be refrigerated
- Avoid exposure to direct sunlight, extreme heat or cold
- Store prefilled syringes upright 1 week if 2 insulin types; 30 days for one
Problems with insulin therapy:
- Hypoglycemia
- Allergic reaction
- Lipodystrophy
Somogyi Effect
- Rebound effect in which an overdose of insulin causes hypoglycemia
- Release of counter-regulatory hormones causes rebound hyperglycemia
- Danger: when BG is measured in the morning, hyperglycemia is present and the patient or healthcare
professional may increase the dose of insulin
Dawn Syndrome
- Morning hyperglycemia present on awakening
- May be due to release of counter-regulatory hormones in predawn hours
- Growth hormone and cortisol
Acute complications of diabetes including DKA, HHS, hypoglycemia
Caused by profound deficiency of insulin
Characterized by
- Hyperglycemia
- Ketosis
- Acidosis
- Dehydration
Most likely to occur in type 1 DM
Less severe form may be treated on outpatient basis
Hospitalize for severe fluid and electrolyte imbalance, fever, N/V, diarrhea, altered mental state
Also if communication with healthcare provider is lacking
Precipitating factors
- Illness
- Infection
- Inadequate insulin dosage
- Undiagnosed type 1 DM
- Poor self-management
- Neglect
Clinical manifestations
- Dehydration
- Poor skin turgor
- Dry mucous membranes
- Tachycardia
- Orthostatic hypotension
- Lethargy and weakness early
- Skin dry and loose; eyes soft and sunken
- Abdominal pain, anorexia, N/V
- Kussmaul respirations
- sweet , fruity breath odor
- BG level of >250 mg/dL
- Blood pH lower than 7.30
- Serum bicarbonate level < 16 mEq/L
- Moderate to high ketone levels in the urine or serum
- Electrolyte imbalances
- Ensure patent airway; administer O2
- Establish IV access; begin fluid restriction
- NaCL 0.45 % or 0.9%
- Add 5% to 10% dextrose when BG level approaches 250 mg/dL
- Continuous regular insulin drip 0.1 U/kg/hr
- Potassium replacement as needed
Hyperosmolar Hyperglycemic Syndrome (HHS)
- Life-threatening syndrome
- Occurs with type 2 DM
- Enough circulating insulin to prevent ketoacidosis but not enough to prevent severe hyperglycemia,
osmotic diuresis and ECF depletion
- Fewer sx in the early stages lead to higher glucose levels ( > 600 mg/dL)
- Medical emergency
- High mortality rate
- Correct underlying precipitating cause
Precipitating factors
- UTI’s, pneumonia, sepsis
- Acute illness
- Newly diagnosed type 2 DM
- Impaired thirst sensation and/or inability to replace fluids
- More severe neurologic manifestations because of increase serum osmolality
- Coma
- Somnolence
- Seizures
- Hemiparesis
- Aphasia
- Ketones absent or minimal in blood and urine
Therapy similar to that for DKA
- IV insulin and NaCl infusions
- More fluid replacement needed
- Monitor serum potassium and replace as needed
- Too much insulin in proportion to glucose in the blood
- Blood glucose level < 70 mg/dL
- Neuroendocrine hormones released
- Autonomic nervous system activated
Hypoglycemia unawareness
- No warning signs/symptoms until glucose level until glucose level critically low
- Related to autonomic neuropathy and lack of counter-regulatory hormones
- Patients at risk should keep blood glucose levels somewhat higher
- Too much insulin or oral hypoglycemic agents
- Too little food
- Delaying time of eating
- Too much exercise
- Sx can also occur when high glucose level falls too rapidly
Check blood glucose level
- If <70 mg/dL, begin tx
- If > 70 mg/dL, investigate further for cause of s/s
- If monitoring equipment not available, tx should be initiated - D5
Chronic complications of diabetes including autonomic neuropathy,
- Damage to the blood vessels secondary to chronic hyperglycemia
- Leading cause of diabetes-related death
- Macrovascular and microvascular
- Tight glucose levels can prevent or minimize complications
Macrovascular Angiopathy
- Diseases of large and medium sized blood vessels
- Greater frequency and earlier onset in patients with DM
- Cerebrovascular disease
- Cardiovascular disease
- Peripheral vascular disease
Decrease risk factors (yearly screening)
- Obesity
- Smoking
- Increases risk for blood and vessel disorders
- High fat intake
- Sedentary lifestyle
Screen for and treat hyperlipidemia
- Normal levels
- LDL → <100
- HDL → >40 (men), >50 (women)
- Triglycerides → <50
Lifestyle changes are important
- Younger than 40 and type 1
- Treat with statins if they have a cardiovascular disease
Microvascular Angiopathy
- Thickening of vessel membranes in capillaries and arterioles in response to chronic
- Specific to DM and includes
- Retinopathy (eyes)
- Nephropathy (kidneys)
- Dermopathy (skin)
- Usually appear 10 to 20 years after diagnosis
Diabetic Retinopathy
- Microvascular damage to retina as a result of chronic hyperglycemia
- Most common cause of new cases of adult blindness
- Nonproliferative: more common
- Partial occlusion of small blood vessels in retina causes micro aneurysms
- Capillary fluids leak out causes edema
- May cause mild to severe vision loss of untreated
- Proliferative: more severe
- Involves retina and vitreous humor
- New blood vessels formed (neovascularization)
- Very fragile and bleed easily
- Can cause retinal detachment
Diabetic Nephropathy
- Damage to small blood vessels that supply the glomeruli of the kidney
- Leading cause of end-stage renal disease
- 20- 40 % of people with DM
- Risk factors
- Accelerates the progression of nephropathy
- Genetics
- Smoking
- Chronic hyperglycemia (uncontrolled)
- Annual screening
- If albuminuria is present, give drugs to delay progression
- ACE inhibitors (lisinopril)
- Angiotensin II receptor antagonists (ex. losartan)
- Control of HTN and BG levels in a healthy range (imperative)
- Measure Serum Creatinine & GFR
Diabetic Neuropathy
- Nerve damage due to metabolic derangements of DM
- 60-70% of patients with DM have some degree of neuropathy
- Reduces nerve conduction and demyelination
- Sensory or autonomic
- Sensory neuropathy
- Loss of protective sensation in lower extremities
- Major risk for amputation
- Risk for infection
- Foot care is important
- Cotton socks
Distal symmetric polyneuropathy
- Most common form
- Affects hands and/or feet bilaterally
- Can cause atrophy of hands and/or feet
- Loss of sensation, abnormal sensations, pain and paresthesia (tingling sensation)
- Treat paresthesia
- Pts with paresthesia are at risk for falls
- Pain is described as “burning”
- Medications don’t always work
Tx for sensory neuropathy
- Managing BG levels
- Drug therapy
- Topical creams
- Capsaicin
- Made from chili peppers
- Tricyclic antidepressants
- Anti-seizure medications
Autonomic Neuropathy
- Can affect nearly all body systems
- Can lead to hypoglycemia unawareness
- Can lead to bowel incontinence
- Delayed gastric emptying is a complication of autonomic neuropathy
- Can produce N/V, GERD, anorexia, persistent feeling of fullness
Cardiovascular abnormalities
- Postural hypotension, resting tachycardia, painless myocardial infarction
Sexual function
- Erectile dysfunction
- Common
- First manifestation of autonomic neuropathy
- Decreased libido
- Depending on age of woman
- Vaginal infections
Neurogenic bladder → urinary retention
- Empty frequently, use Crede’s maneuver
- Medications (cholinergic agonists)
- Self-catheterization
Foot complications
- Microvascular and macrovascular diseases increases risk for injury and infection
- Sensory neuropathy and PAD are major risk factors for amputation
- Also clotting abnormalities, impaired immune function, autonomic neuropathy
- Smoking increases risk
- Sensory neuropathy
- Loss of protective sensation → unawareness of injury
- Monofilament screening
- Thin filament is swiped across the plantar of the foot to see if there is any
- Insensitivity increases risk for ulcers
- Peripheral artery disease (PAD)
Decreased blood flow
- Decreased wound healing
- Increased risk for infection
- Patient teaching is important to prevent foot ulcers
- Proper footwear
- Prescription shoes
- Avoidance of foot injury
- Skin and nail care
- Daily inspection of feet
- Prompt treatment of small problems
- Diligent wound care for foot ulcers
- Neuropathic arthopathy (Charcot’s foot)
- Leads to joint dysfunction
- Read in textbook !!!!
Prevailing theory **** READ IN BOOK***
● The prevailing theory is that persistent hyperglycemia leads to an accumulation of sorbitol and
fructose in the nerves that causes damage by an unknown mechanism. The result is reduced nerve
conduction and demyelinization. Ischemic damage by chronic hyperglycemia in blood vessels that
supply the peripheral nerves is also implicated in the development of diabetes-related neuropathy.
Neuropathy can precede, accompany, or follow the diagnosis of diabetes.
Skin Problems
- Diabetic dermopathy
- Most common
- Red brown, round or oval patches
- Acanthosis nigricans
- Manifestation of insulin resistance
- Velvety light brown to black skin
- Necrobiosis lipoidica diabeticorum
- Red yellow lesions
- Defect in mobilization of inflammatory cells and impaired phagocytosis
- Recurring or persistent infections
- Candida albicans, boils
- Treat promptly and vigorously
- Patient teaching for prevention
- Hand hygiene
- Flu and pneumonia vaccine
Fluids and Electrolytes
Chapter 16
Mechanisms controlling fluid and electrolyte movement
● v Diffusion
● Movement of molecules across a permeable membrane from high to low concentration
● Net movement of molecules stops when the concentrations are equal in both areas
● It occurs in liquids, gases, & solids
● Simple diffusion requires NO external energy
● v Facilitated Diffusion
● Uses protein carriers to assist moving large molecules from an area of high to low concentration
● Like simple diffusion, facilitated diffusion is passive and requires NO energy (example: glucose transport
into a cell)
● v Active Transport
● Process in which molecules move against concentration gradient
● External energy is required for this process (example: sodium-potassium pump)
● Active transport requires energy (ATP) to move electrolytes against the concentration gradient into
the cell membrane.
● v Osmosis
● Osmosis is the pulling of water into and out of the cells by osmotic pressure
● Movement of water “down” concentration gradient
● From a region of low solute concentration to one of high solute concentration
● Across a semipermeable membrane
● Requires no outside energy source
● Whenever dissolved substances are contained in a space with a semipermeable membrane, they can
pull water into the space by osmosis
The concentration of the solution determines the strength of the of the osmotic pull
The higher the concentration, the greater a solution’s pull, or osmotic pressure
It is the amount of pressure required to stop osmotic flow of water
Osmolarity measures the total milliosmoles/L of solution
Osmolality measures the number of milliosmoles/kg of water
Osmotic Movement of Fluids
Isotonic: fluids with the same osmolality as the cell interior. ECF & ICF are isotonic to one another, so no net
movement of water occurs
Hypotonic: solutions in which the solutes are less concentrated than in the cells.
● If a cell is surrounded by hypotonic fluid, water moves into the cell, causing the cell to swell and possibly
Hypertonic: fluids with solutes more concentrated than in cells, or and increased osmolality
● If hypertonic fluid surrounds a cell, water leaves the cell to dilute ECF; the cell shrinks and may
eventually die
v Hydrostatic Pressure
● Is the force of fluid in a compartment pushing against a cell membrane or vessel wall
● In the blood vessels, hydrostatic pressure is the BP generated by the contraction of the heart
● In the vascular system hydrostatic pressure decreases as the blood moves through the arteries
● At the capillary level, hydrostatic pressure is the major force that pushes water out of the vascular
system & into the interstitial spacet
Oncotic Pressure
● Osmotic pressure (colloid osmotic pressure) caused by plasma proteins
● The major colloids in the vascular system contributing to osmotic pressure are proteins, such as albumin
Fluid Shifts
● If capillary or interstitial pressures change, fluid may abnormally shift from one compartment to another,
resulting in edema or dehydration
● Shifts of Plasma to Interstitial Fluid: Edema, an accumulation of fluid in the interstitial space. Occurs if:
● Venous hydrostatic pressure rises
● Plasma oncotic pressure decreases
● Or interstitial oncotic pressure rises
● Elevation of Venous Hydrostatic Pressure: Edema due to increasing pressure at the venous end of the capillary
which inhibits fluid movement back into the capillary. Causes include:
● Fluid overload
● Heart failure
● Liver failure
● Obstruction of venous return to the heart (ex: restrictive clothing, tourniquets, venous thrombosis)
● Venous insufficiency (ex. varicose veins)
● Decrease in Plasma Oncotic Pressure: fluid remain in interstitial space if the plasma oncotic pressure is
too low to draw fluid back into the capillary.
Low plasma protein content decreases oncotic pressure. Can result from:
● Excessive protein loss (renal disorders)
● Deficient protein synthesis (liver disease)
● Deficient protein intake (malnutrition)
● Elevation of Interstitial Oncotic Pressure: trauma, burns, & inflammation can damage capillary walls and allow
plasma proteins to accumulate in the interstitial space
● This increases interstitial oncotic pressure, draws fluid into the interstitial space, & holds it there
● Fluid Spacing
● Describes the distribution of body water
● First spacing: Normal distribution of fluid (ICF & ECF)
● Second spacing: Abnormal accumulation of interstitial fluid (edema)
● Third spacing: occurs when excess fluid collects in the nonfunctional area between cells. Fluid is trapped
where it is difficult or impossible for it to move back into cells or blood vessels. Occurs in:
● Ascites
● Fluid leaking into the abdominal cavity with peritonitis or pancreatitis
● edema associated with burns trauma or sepsis
Regulation of water balance
• Insensible water loss, which is invisible vaporization from the lungs and skin, assists in regulating body temperature.
Accelerated body metabolism, which occurs with increased body temperature and exercise, increases the amount of
water lost and may result in the need for additional water replacement.
• Normal fluid balance in an adult:
Hypothalamic-pituitary regulation
Osmoreceptors in hypothalamus sense fluid deficit or increase
Deficit stimulates thirst and antidiuretic hormone (ADH) release
ADH acts on the distal tubules and collecting ducts in the kidney making them more permeable to water, the
result is increased water reabsorption from the tubular filtrate into the blood and decreased excretion in the
Decreased plasma osmolality (water excess) suppresses ADH release
Renal regulation
○ Primary organs for regulating fluid and electrolyte balance by adjusting urine volume and excretion of
most electrolytes
○ With severely impaired renal function, the kidneys cannot maintain fluid and electrolyte balance - this
condition results in edema, potassium and phosphorus retention, acidosis and other electrolyte
○ Adjusting urine volume
○ Selective reabsorption of water and electrolytes
○ Renal tubules are sites of action of ADH and aldosterone
Adrenal cortical regulation
○ Releases hormones to regulate water and electrolytes
○ Glucocorticoids - primarily have an anti-inflammatory effect and increase serum glucose levels
○ Cortisol - most abundant glucocorticoid. In large doses, cortisol has both glucocorticoid (glucoseelevating and antiinflammatory) and mineralocorticoid (sodium-retention) effects. Normally cortisol
secretion is in a diurnal or circadian pattern. Increased cortisol secretion occurs in response to physical
and psychologic stress.
○ Mineralocorticoids - enhance sodium retention and potassium secretion
○ Aldosterone - a mineralocorticoid with strong sodium-retaining and potassium- excreting capabilities.
Decreased renal perfusion or decreased sodium in the distal portion of the renal tubule activates the
renin-angiotensin-aldosterone system (RAAS), resulting in aldosterone secretion.
○ In addition to the RAAS, increased serum potassium, decreased serum sodium, and adrenocorticotropic
hormone (ACTH) stimulate aldosterone secretion. Aldosterone increases sodium and water reabsorption
in the renal distal tubules, decreasing plasma osmolality and restoring fluid volume.
Cardiac regulation
○ Natriuretic peptides are antagonists to the RAAS
○ They are produced by cardiomyocytes in response to increased atrial pressure
○ They are natural antagonists to the RAAS and suppress secretion of aldosterone, renin, and ADH to
decrease blood volume and pressure
Gastrointestinal regulation
○ Oral intake accounts for most water
○ The GI tract normally secretes around 8000 mL of digestive fluids each day
○ Small amounts of water are eliminated by gastrointestinal tract in feces
○ Diarrhea and vomiting can lead to significant fluid and electrolyte loss
○ Gerontologic considerations
○ structural changes in kidneys decrease ability to conserve water
○ Hormonal changes include a decrease in renin and aldosterone and increase in ADH and ANP
○ Loss of subcutaneous tissue leads to increased moisture lost
Causes of Volume Imbalances
○ Abnormal gastrointestinal (GI) losses: Vomiting, nasogastric suctioning, diarrhea
○ Abnormal skin losses: Diaphoresis
○ Abnormal renal losses: Diuretic therapy, diabetes insipidus,
○ kidney disease, adrenal insufficiency, osmotic diuresis
○ Third spacing: Peritonitis, intestinal obstruction, ascites, burns
○ Hemorrhage
○ Altered intake, such as nothing by mouth (NPO)
Extracellular Fluid Imbalances
Fluid and electrolyte imbalances occur to some degree in most patients with a major illness or injury because
illness disrupts normal homeostatic mechanisms. Illness or disease directly causes some fluid and electrolyte
imbalances (e.g., burns, heart failure).
● Other times therapeutic measures (e.g., colonoscopy preparation, diuretics) cause or contribute to imbalances.
● Perioperative patients are at risk for developing fluid and electrolyte imbalances because of fluid restrictions,
blood or fluid loss, and the stress of surgery.
● Fluid volume deficits can be divided into two main categories: volume imbalances and osmolality imbalances.
● When there is an issue with volume imbalance, it relates to a lack of body fluid in the extracellular
● Osmolality imbalances occur when there is disturbance in concentration of body fluid.
● Volume imbalances occur when too little or too much isotonic fluid is present.
● Osmolality imbalances occur when body fluid becomes either hypertonic or hypotonic.
● Hypernatremia (water deficit) and hyponatremia (water excess or intoxication) are good examples of this type of
ECF volume deficit (hypovolemia)
● Abnormal loss of body fluids, inadequate fluid intake, or plasma to interstitial fluid shift
● Fluid volume deficit can occur with abnormal loss of body fluids (e.g., diarrhea, vomiting, hemorrhage, polyuria),
inadequate fluid intake, or a plasma to interstitial fluid shift
● Clinical manifestations related to loss of vascular volume as well as CNS effects
● Deficient fluid volume
● Decreased cardiac output
● Risk for impaired oral mucous membranes
● Potential complication: Hypovolemic shock
● Vital Signs: Hyperthermia, tachycardia (in an attempt to maintain a normal blood pressure), thready pulse,
hypotension, orthostatic hypotension, decreased central venous pressure, tachypnea (increased respirations to
compensate for lack of fluid volume within the body), hypoxia
● Neuromusculoskeletal: Dizziness, syncope, confusion, weakness, fatigue
● Gastrointestinal: Thirst, dry furrowed tongue, nausea, vomiting, anorexia, acute weight loss
● Renal: Oliguria (decreased production and concentration of urine)
● Other: Diminished capillary re ll, cool clammy skin, diaphoresis, sunken eyeballs, attened neck veins, poor skin
turgor and tenting, weight loss, low central venous pressure
Interprofessional Care
● Correct the underlying cause and replace water and electrolytes
● Orally - in mild losses
● Blood products - when volume loss is due to blood loss
● Balanced IV solutions - such as isotonic (0.9%) sodium chloride or lactated ringers solution
Fluid volume excess (hypervolemia)
● Excess intake of fluids, abnormal retention of fluids, or interstitial-to-plasma fluid shift
● Clinical manifestations related to excess volume
● Excess fluid volume
● Impaired gas exchange
● Risk for impaired skin integrity
● Activity intolerance
● Disturbed body image
Potential complications: Pulmonary edema, ascites
Vital Signs: Tachycardia, bounding pulse, hypertension, tachypnea, increased central venous pressure
Neuromuscular: Weakness due to excess fluid retained, which depletes energy and increases the workload for
the body; headache; altered level of consciousness
● Gastrointestinal: Ascites
● Respiratory: Crackles, cough, increased respiratory rate, dyspnea caused from an excess of fluids within the body
and lungs
● Other: Peripheral edema due to an excess of fluids within the body and lungs, resulting in weight gain, distended
neck veins, and increased urine output
● Inter-professional Care
○ Remove fluid without changing electrolyte composition or osmolality of ECF
■ Diuretics
■ Fluid restriction
■ Restriction of sodium intake to treat ascites or pleural effusion
● Nursing Implementation
○ Daily weights - most accurate measure of volume status, an increase of 1 kg (2.2 lb) is equal to 1000 mL
(1 L) of fluid retention
○ I&O
○ Laboratory findings
○ the patient with a fluid volume deficit often has increased BUN, sodium, and hematocrit levels with
increased plasma and urine osmolality.
○ With fluid volume excess, the patient will have decreased BUN, sodium, and hematocrit levels with
decreased plasma and urine osmolality.
● Cardiovascular care * priority
○ Changes in BP, central venous pressure, pulse force, and jugular venous distention reflect ECF volume
○ In fluid volume excess, the pulse is full, bounding, and not easily obliterated. Increased volume causes
distended neck veins (jugular venous distention), increased central venous pressure, and high BP.
Auscultate heart sounds, being alert for the presence of an S3.
● Respiratory care
○ Monitor pulse oximetry and auscultate lung sounds as needed.
○ ECF excess can result in pulmonary congestion and pulmonary edema, as increased hydrostatic pressure
in the pulmonary vessels forces fluid into the alveoli.
○ The patient will experience shortness of breath and moist crackles on auscultation.
○ The patient with ECF deficit will demonstrate an increased respiratory rate because of decreased tissue
perfusion and resultant hypoxia. Administer oxygen as ordered.
● Patient safety
○ The patient with fluid volume deficit is at risk for falls because of orthostatic hypotension, muscle
weakness, and changes in level of consciousness. Assess level of consciousness, gait, and muscle
strength. Implement fall precautions.
• Skin care: assess skin turgor
Question: (Answer = A)
In a patient with prolonged vomiting, the nurse monitors for fluid volume deficit because vomiting results in
a. Fluid movement from the cells into the interstitial space and the blood vessels
b. Excretion of large amounts of interstitial fluid with depletion of extracellular fluids
c. An overload of extracellular fluid with a significant increase in intracellular fluid volume
d. Fluid movement from the vascular system into the cells, causing cellular swelling and rupture
Manifestations, normal ranges, and nursing management for:
Hypo- and hypernatremia
● Sodium (Na+) - Normal Ranges = 135-145 mEq/L
● Imbalances are typically associated with parallel changes in osmolality
● Sodium plays a major role in:
■ ECF volume and concentration
■ Generation and transmission of nerve impulses
■ Muscle contractility
■ Acid-base balance
■ Serum sodium level reflects the ratio of sodium to water, not necessarily the amount of sodium
in the body.
■ Changes can reflect a primary water imbalance, primary sodium imbalance, or combination of
the two.
● Hyponatremia - ( Na+ < 135 mEq/L) - Usually associated with ECF hypoosmolality from the excess water.
To restore balance, fluid shifts out of the ECF and into the cells (ICF), leading to cellular edema.
■ Manifestations of hyponatremia are due to cellular swelling and first appear in the CNS.
● Mild Hyponatremia symptoms: headache, irritability, and difficulty concentrating
● Severe Hyponatremia symptoms: Confusion, vomiting, seizures, and coma. Irreversible
neurological damage or death from brain herniation can occur.
● Vital Signs: Hypothermia, tachycardia, rapid thready pulse, hypotension, orthostatic
hypotension, diminished peripheral pulses.
● Neuromusculoskeletal: lethargy, muscle weakness to the point of possible respiratory
compromise, fatigue, decreased deep-tendon reflexes (DTRs), seizures, lightheadedness,
● Gastrointestinal: Increased motility, hyperactive bowel sounds, abdominal cramping,
■ Nursing Management:
● Managing hyponatremia from fluid loss includes replacing fluid using isotonic sodiumcontaining solution, encouraging oral intake, and withholding all diuretics.
● Mild hyponatremia caused by water excess, fluid restriction is often the only
treatment. Loop diuretics may be given.
● Acute or more serious hyponatremia- small amounts of IV hypertonic saline solution
(3% NaCl) can restore the serum sodium level. Monitor for shortness of breath and
increased respiratory rate.
● Vasopressor receptor antagonists (drugs that block the activity of ADH), are uses to
treat patients who cannot tolerate fluid restrictions and have more severe symptoms.
These drugs include conivaptan (Vaprisol) and tolvaptan (Samsca). They promote
excretion of excess fluid.
● Replacement of sodium should not exceed more than 8 to 12 mEq/L in a 24-hr period
because rapid rise in sodium level risks development of neurological damage due to
● Monitor I&O
● Hypernatremia- (Na+ > 145 mEq/L) - May occur with inadequate water intake, excess water loss, or
rarely, sodium gain. Hypernatremia causes hyperosmolality. ECF hyperosmolality causes water to move
out of the cells to restore equilibrium, leading to cellular dehydration.
■ Primary protection is thirst from hypothalamus.
■ Manifestations:
● Thirst
● Alterations of mental status, ranging from agitation, restlessness, confusion, and
lethargy to seizures and coma
● Symptoms of fluid volume deficit
● Vital signs: hyperthermia, tachycardia, orthostatic hypotension
● Neuromusculoskeletal: Restlessness, irritability, muscle twitching to the point of muscle
weakness, including respiratory compromise; decreased or absent DTRs
● Gastrointestinal: dry mucous membranes, nausea, vomiting, anorexia, occasional
■ Nursing Management:
● Treat underlying cause
● Primary water deficit- replace fluid orally or IV with isotonic or hypotonic fluids
● Excess sodium- dilute with sodium-free IV fluids and promote excretion with diuretics
(5% dextrose in water).
● Serum sodium levels should not decrease by more than 8 to 15 mEq/L in an 8-hour
period. Quickly reducing levels can cause a rapid shift of water back into the cells,
resulting in cerebral and/or pulmonary edema and neurologic complications.
Hypo- and hyperkalemia
● Potassium (K+)- Normal Ranges= 3.5-5.0 mEq/L
● Major ICF cation
● Necessary for:
■ Transmission and conduction of nerve and muscle impulses
■ Cellular growth
■ Maintenance of cardiac rhythms
■ Acid-base balance
■ Regulated by kidneys
■ Diet is the source of potassium
● Hypokalemia- (K+ <3.5 mEq/L) - Most common causes are abnormal losses from either the kidneys or GI
■ Clinical Manifestations:
● Fatigue
● Muscle weakness, leg cramps
● Soft, flabby muscles
● Paresthesias (pins and needles), decreased reflexes
● Constipation, nausea, paralytic ileus
● Shallow respirations
● Weak, irregular pulse
● Hyperglycemia
● Decreased blood pressure
● Altered mental status, anxiety, confusion
■ Most serious are Cardiac changes:
● Impaired repolarization resulting in flattened T wave
● Depressed ST segment
● Presence of a U wave.
● Prolonged PR interval
● Nurse should be concerned with drugs like digoxin
Nursing Management:
● Oral or IV potassium chloride (KCl) supplements and increasing dietary intake of
○ Always dilute IV KCL
○ NEVER give KCL via IV push or as a bolus
○ Should not exceed 10 mEq/hr
○ Use an infusion pump
○ It is irritating to the veins and can burn tissues
○ Potassium rich foods and sources:
■ Fruits and vegetables (bananas and oranges)
■ Salt substitutes
■ Stored blood
● Hyperkalemia- (K+ >5.0 mEq) - May result from impaired renal excretion, shift of potassium from ICF to
ECF, a massive intake of potassium, or combination. Most common cause is renal failure.
● Acidosis: massive fluid loss (ex. Burns, crushed injury), potassium is released from cells into the
intravascular system therefore they’re high levels of K
● Medications such as heparin, angiotensin 2 receptors, ACE inhibitors: prevent K excretion which
increases the levels.
■ Clinical manifestations:
● Fatigue, irritability
● Weak or paralyzed skeletal muscles, cramping leg pain
● Cardiac dysrhythmias, Disturbances in cardiac conduction
○ Heart block, ventricular fibrillation
● Loss of muscle tone
● Paresthesias, decreased reflexes
● Abdominal cramping, diarrhea, vomiting
● Confusion
● Irregular pulse
● Tetany (intermittent muscle spasms)
■ Nursing Management:
● Force K from ECF to ICF by IV insulin and a �- adrenergic agonist or sodium bicarbonate
(if patient is acidotic)
● Reverse membrane effects of elevated ECF potassium by administering calcium
gluconate IV (Stabilizes cardiac membranes and protects from dysrhythmias)
● Increase elimination of potassium (via loop or thiazide diuretics, dialysis)
Hypo- and hypercalcemia
Calcium( Ca2+)- Normal Ranges= 8.6-10.2 mg/dL
● Functions:
● Formation of teeth and bone
● Blood clotting
● Transmission of nerve impulses
● Myocardial contractions
● Muscle contractions
● Hypocalcemia -(Ca2+ <8.6 mg/dL) - Caused by: Decreased production of PTH (parathyroid hormone), multiple
blood transfusions, alkalosis, increased calcium loss
● Clinical Manifestations:
■ Tetany is most common manifestation in hypocalcemia state.
■ Positive Trousseau’s sign
● Hand/finger spasms with sustained blood pressure cuff inflation
■ Positive Chvostek’s sign
● Tapping on the facial nerve triggering facial twitching
■ Laryngeal stridor
■ Dysphagia
■ Tingling around the mouth or in the extremities
■ Cardiac dysrhythmias
■ Seizures
■ Potential complication: Fracture, respiratory arrest
■ Decreased BP
● Nursing Management:
■ Treat cause
■ Oral or IV calcium supplements
■ Rebreathe into paper bag
■ Treat pain and anxiety to prevent hyperventilation- induced respiratory alkalosis
■ Measures to promote CO2 retention
Hypercalcemia- (Ca2+ >10.2 mg/dL)- Caused by hyperparathyroidism (⅔ of cases), or malignancies. Prolonged
immobilization can also cause hypercalcemia.
○ Clinical Manifestations:
■ Fatigue, lethargy, weakness, confusion
■ Hallucinations, seizures, coma
■ Cardiac dysrhythmias: Heart block and ventricular tachycardia
■ Increased BP
■ Bone pain, fractures, nephrolithiasis
■ Polyuria, dehydration
○ Nursing Management:
■ Excretion of Ca with loop diuretic
■ Hydration with isotonic saline infusion (.9%)
■ Low calcium diet
■ Ingestion of 3000-4000 mL of fluid daily
■ Mobilization (ambulation; PROM)
■ Bisphosphonates (interfere with activity of osteoclasts)
■ IM or SC calcitonin (increases renal excretion)
Hypo- and hyperphosphatemia
● Phosphate (PO43-)- Normal Ranges= 2.4-4.4 mg/dL
● Primary anion in ICF
● Essential to function of muscle, red blood cells, and nervous system
Involved in acid-base buffering system, ATP production, cellular uptake of glucose, and metabolism of
carbohydrates, proteins, and fats
● Serum levels controlled by parathyroid hormone
● Maintenance requires adequate renal functioning
● Reciprocal relationship with calcium.
○ Low calcium level stimulates the release of PTH, decreasing reabsorption of phosphorus and lowering
phosphorus levels.
● Hypophosphatemia -(PO43- <2.4 mg/dL)- Can result from decreased intestinal absorption, increased urinary
excretion, or from ECF to ICF shifts. Malabsorption, diarrhea, and phosphate-binding antacids lead to decreased
absorption. Inadequate replacement during parenteral nutrition.
○ Clinical Manifestations:
■ CNS depression
■ Muscle weakness and pain
■ Respiratory and heart failure
■ Rickets and osteomalacia (because of altered bone metabolism)
■ Rhabdomyolysis
■ Seizures
○ Nursing Management:
■ Oral supplementation
■ Ingestion of foods high in phosphorus (ex. dairy)
■ IV administration of sodium or potassium phosphate
● Hyperphosphatemia-( PO43- >4.4 mg/dL) - Common in patients with acute kidney injury or chronic kidney
● A phosphate shift from ICF to ECF.
● Chemotherapy
● Excess intake of phosphate or vitamin D
● Hypoparathyroidism
○ Clinical Manifestations:
■ Neuromuscular irritability and tetany (hypocalcemia)
■ Calcified deposition in soft tissue such as joints, arteries, skin, kidneys, and corneas (can cause
organ dysfunction)
○ Nursing Management:
■ Treat underlying cause
■ Restrict foods (ex. Dairy products) and fluids containing phosphorus
■ Oral phosphate-binding agents (calcium carbonate)
■ Volume expansion and forced diuresis
■ Correct any hypocalcemia
■ Hemodialysis
Hypo- and hypermagnesemia
● Magnesium (Mg+)- Normal Ranges= 1.5-2.5 mEq/L
● Coenzyme in metabolism of carbohydrates
● Required for DNA and protein synthesis
● Blood glucose control
● BP regulation
● Necessary for ATP production
● Acts directly on myoneural junction (muscle contraction and relaxation)
Important for normal cardiac function
Absorbed by GI tract, excreted by kidneys
Manifestations of magnesium imbalances are often mistake for calcium imbalances
Hypomagnesemia- (Mg+ <1.5 mEq/L)- Caused by prolonged fasting or starvation and chronic alcoholism.
Prolonged parenteral nutrition without magnesium supplementation, fluid loss from GI tract, diuretics and
hyperglycemic osmotic diuresis are also causes.
○ Clinical manifestations:
■ Hypomagnesemia resembles hypocalcemia
■ Hyperactive deep tendon reflexes
■ Muscle cramps
■ Tremors
■ Seizures
■ Increased Pulse, Increase BP
■ Cardiac dysrhythmias
● Associated with digitalis toxicity
■ Chvostek’s and Trousseau’s sign
■ Confusion, seizures, vertigo
■ GI- constipation, hypoactive bowel sounds, paralytic ileus
○ Nursing Management:
■ Treat underlying cause
■ Oral supplements
■ Increase dietary intake (diary products)
■ Parenteral IV or IM magnesium when severe
● Slow infusion due to rapid administration can lead to hypotension and cardiac or
respiratory arrest.
Hypermagnesemia- (Mg+ > 2.5 mEq/L)- Usually occurs with increased magnesium intake when renal
insufficiency or failure is present. Excess IV magnesium administration can also cause hypermagnesemia.
○ Clinical manifestations:
■ Lethargy
■ Nausea and vomiting
■ Impaired reflexes
■ Muscle paralysis
■ Respiratory and cardiac arrest
■ Decreased Pulse, Decreased BP
○ Nursing Management:
■ Prevention first- restrict magnesium intake in high-risk patients
■ IV calcium chloride or calcium gluconate if symptomatic
■ Fluids and IV furosemide (diuretic) to promote urinary excretion
■ Dialysis
Renal Disorders (Chapters 45, 46, & 54)
Acute vs chronic renal failure
Acute Kidney Injury:
● Acute Kidney Injury (AKI) is the term used to encompass the entire range of the syndrome, including a very slight
deterioration in kidney function to severe impairment.
● AKI is characterized by a rapid loss of kidney function. This loss is accompanied by a rise in serum creatinine level
&/or a reduction in urine output. The severity of dysfunction can range from a small increase in serum creatinine
or reduction in urine output to the development of azotemia (an accumulation of nitrogenous waste products
[urea nitrogen, creatinine] in the blood.)
● AKI can develop over hours/days with progressive elevations of BUN, creatinine, & potassium, with or without a
reduction in urine output.
● Prerenal causes
○ Factors that reduce systemic circulation -> reduction in renal blood flow -> decreased glomerular
perfusion & filtration of the kidneys
○ Prerenal oliguria
■ no damage to the kidney tissue (parenchyma)
■ caused by a decrease in circulating blood volume (i.e. severe dehydration, HF, ↓ CO)
■ Readily reversible with appropriate treatment
○ Autoregulatory mechanisms that ↑ angiotensin II, aldosterone, norepinephrine, & antidiuretic hormone
attempt to preserve blood flow to essential organs
○ Prerenal azotemia results in a reduction in the excretion of Na (<20 mEq/L), increased Na & H2O
retention, & ↓ urine output.
○ Can lead to intrarenal AKI
● Intrarenal (intrinsic) causes
○ Conditions that cause direct damage to the kidney tissue, resulting in impaired nephron function
○ Damages from intrarenal causes result from:
■ prolonged ischemia
■ nephrotoxins (i.e aminoglycoside antibiotics, contrast media)
● Can crystallize or cause damage to the epithelial cells of the tubules
hemoglobin (released from hemolyzed RBCs) & myoglobin (released from necrotic muscle cells)
● Can block the tubules & cause renal vasoconstriction
○ Glomerulonephritis & systemic lupus erythematosus may cause AKI
○ Acute tubular necrosis (ATN)
■ Most common intrarenal cause of AKI
■ Primarily result of
● Ischemia
○ Causes a disruption in the basement membrane & patchy destruction of the
tubular epithelium
● Nephrotoxins
○ Cause necrosis of tubular epithelial cells - slough off & plug the tubules
● Sepsis
■ Potentially reversible if basement membrane is not destroyed & tubular epithelium regenerates
Postrenal causes
○ Involve mechanical obstruction in the outflow of urine
■ Urine refluxes into the renal pelvis -> impairing kidney function
○ Most common postrenal causes:
■ Prostate cancer
■ Calculi
■ Trauma
■ Extrarenal tumors
○ Bilateral ureteral obstruction leads to
■ hydronephrosis (kidney dilation)
■ ↑ in hydrostatic pressure
■ Tubular blockage
■ Progressive decline in kidney function
Risk factors
● Dehydration from
● Age - older adults
● Polypharmacy - diuretics, laxatives, drugs that suppress appetite/consciousness
● Acute febrile illness
● Immobility (bedridden)
● Less volume/fluids to work with… kidneys work harder
● Hypotension
● Diuretic therapy
● Aminoglycoside therapy
● Obstructive disorders (i.e. prostatic hyperplasia)
● Surgery
● Infection
Clinical manifestations
AKI may progress through phases:
● Oliguric phase
○ Common manifestation
○ <400 mL/day
○ Usually occurs within 1-7 days of the injury to kidneys
○ If on nephrotoxic drugs, oliguria can be delayed
○ Change in urine output doesn’t correspond to changes in GFR
○ Commonly seen with prerenal causes
● Diuretic phase
○ Daily urine output is about 1-3L, may reach 5+ L
○ Nephrons are still not fully functional even as urine output increases
○ High urine volume is caused by osmotic diuresis from high urine concentration in the glomerular
filtrate & the inability of the tubules to concentrate the urine
○ Kidneys have recovered the ability to excrete, but not concentrate the urine
○ May last 1-3 weeks
● Recovery phase
○ GFR increases
○ BUN & serum creatinine levels decrease
○ First 1-2 weeks of phase -> major improvements
○ Those who recover may achieve clinically normal kidney function but remain in an early stage of
When a patient does not recover from AKI, the CKD may develop.
RIFLE Classification
Diagnostic studies:
● Through Hx
○ Essential for diagnosing the etiology of AKI
● Serum creatinine
○ Serum creatinine increase may not be evident until there is a loss of > 50% of kidney function
○ Urine sediment containing abundant cells, casts, or proteins suggests intrarenal disorders
○ The urine osmolality, sodium content, & specific gravity help in differentiating the causes of AKI
○ Urine sediment may be normal in both prerenal & postrenal AKI
○ In intrarenal problems - hematuria, pyuria, & crystals may be seen
● Kidney ultrasonography
○ Often the first test done
○ Provides imaging without exposure to potentially nephrotoxic contrast agents
○ Useful for evaluating for possible kidney disease & obstruction of the urinary collection system
● Renal scan
○ Can assess abnormalities in kidney blood flow, tubular function, & the collecting system
● CT scan
○ Can identify lesions, masses, obstructions, & vascular anomalies
● Renal biopsy
○ Best method for confirming intrarenal causes of AKI
● Contraindicated
○ MRI with gadolinium contrast medium
○ Magnetic resonance angiography (MRA) with gadolinium contrast medium
■ Nephrogenic systemic fibrosis
■ Contrast-induced nephropathy (CIN)
● Can occur when contrast medium for diagnostic studies causes nephrotoxic injury
○ Administration of gadolinium can be potentially fatal in patients with kidney failure
● Ensure adequate intravascular volume & cardiac output
○ Force fluids
○ Loop diuretics (i.e Furosemide/Lasix)
○ Osmotic diuretics (i.e Mannitol)
■ If AKI is already established, forcing fluids & diuretics will not be effective & may be harmful
● Closely monitor fluid intake during oliguric phase
● Management includes:
○ Treatment of precipitating cause
○ Fluid restriction (600 mL + previous 24-hr fluid loss)
○ Nutritional therapy
○ Adequate protein intake (0.6-2 g/kg/day) depending on degree of catabolism
○ Enteral nutrition
○ Parenteral nutrition
○ Dietary restrictions (Potassium, phosphate, sodium)
○ Measures to lower potassium (if elevated)
○ Calcium supplements/phosphate-binding agents
○ Initiation of dialysis (if necessary)
○ Continuous renal replacement therapy (if necessary)
● Temporary therapies for elevated Potassium levels by promoting a transient shift of potassium into the cells ->
hyperkalemia is one of the most serious complications of AKI… can cause life-threatening cardiac dysrhthmias
○ Regular insulin IV
○ Sodium bicarbonate
Calcium gluconate IV (used in advanced cardiac toxicity) -> raises threshold at which dysrhythmias occur
& serves to temporarily stabilize myocardium
Sodium Polystyrene Sulfonate (Kayexalate) -> remove potassium from body… never give to patient with
a paralytic ileus because bowel necrosis can occur
Patiromer (Veltassa)
Dietary therapy
Maintain adequate caloric intake to prevent catabolism (30-35 kcal/kg)
● Primarily carbohydrates & fat
● Limit protein (0.8-1.0 g of protein per kg of desired body weight)
Restrict sodium to prevent edema, HTN, & heart failure
Increase dietary fat (receive at least 30-40% of total calories from fat)
● Fat emulsion IV infusions given as a nutritional supplement to provide a good source of nonprotein
● Prevents ketosis
Enteral nutrition is given if a patient cannot maintain adequate oral intake
Parenteral nutrition is necessary if the GI tract is not functional
● May need daily HD or CRRT to remove excess fluid
Chronic Kidney Disease:
Disease staging:
Based on decrease in GFR <60 for longer than 3 months
o Normal GFR: 125 reflected by urine creatinine clearance
Last stage of kidney failure
o End-stage renal disease occurs when GFR < 15 mL/min
Defined as one of the following:
- Kidney damage
o Pathologic abnormalities
o Markers of damage
- Blood, urine, imaging tests
o < 60 mL/min for longer than 3 months
At this point, renal replacement therapy (dialysis or transplantation) is
required to maintain life
Risk Factors
● DM (most common)
● HTN (most common)
● Glomerulonephritis
● Cystic diseases
● Urologic diseases
● Aging populations >60
● Rise in rates of obesity
● Cardiovascular disease
● Family history of CKD
● Ethnic minority
○ African american
○ Native american
Clinical manifestations
● patients with CKD are first frequently asymptomatic
● Result of retained substances
○ Urea
○ Creatinine
○ Phenols
○ Hormones
○ Electrolytes
○ Water
● Metabolic disturbances
■ Waste product accumulation
● As GFR decreases, BUN and serum creatinine levels increases
○ Serum creatinine clearance (which calculates GFR) determinations are
considered more accurate indicators of kidney function that BUN and
■ BUN level increases
● Not only from kidney failure but also from protein intake, fever, corticosteroids, and
● N/V, lethargy, fatigue, impaired thought processes, and headaches occur
● Significant elevations in BUN contribute to development of nausea, vomiting,
lethargy, fatigue, impaired thought processes, and headaches.
■ Altered carbohydrate metabolism
● Caused by impaired glucose metabolism
■ Elevated triglycerides
● Electrolyte/acid-base imbalances
○ Potassium
■ Hyperkalemia
● Most serious electrolyte disorder in kidney disease
● Results from decreased excretion of potassium by the kidneys, the breakdown of
cellular protein, bleeding, and metabolic acidosis.
■ Fatal dysrhythmias
● When serum potassium level reaches 7 to 8 mEq/L
■ Potassium may also come from the foods, dietary supplements, drugs, and IV infusions.
○ Sodium
■ May be elevated, normal, or low
■ Because of impaired excretion, sodium along with water is retained
● Sodium retention can contribute to edema, HTN, and HF
■ Dilutional hyponatremia may occur
● Edema
● HF
■ If large quantities of water are retained, dilutional hyponatremia occurs.
■ Sodium intake must be individually determined but is generally restricted to 2 g/day.
○ calcium and phosphate alterations
○ magnesium alterations
■ Hypermagnesemia
generally, not a problem unless the patient is ingesting magnesium
■ milk of magnesia
■ magnesium citrate
■ antacids containing magnesium
○ Clinical manifestations
■ absence of reflexes
■ decreased mental status
■ cardiac dysrhythmias
■ Hypotension
■ respiratory failure
● metabolic acidosis
○ results from
■ kidney’s impaired ability to excrete excess acid (primary ammonia)
■ defective reabsorption and regeneration of bicarbonate
○ plasma bicarbonate level usually falls to approximately 16 to 20 mEq/L
■ average adult produces 80 to 90 mEq of acid per day which is normally buffered by
■ plasma bicarbonate is an indirect measure of acidosis
■ decreased plasma bicarbonate reflects its use in buffering metabolic acids
■ The bicarbonate level generally does not progress below this level because hydrogen
ion production is usually balanced by buffering from demineralization of the bone (the
phosphate buffering system).
o Hematologic system
● Anemia (normocytic, normochromic)
○ Due to decreased production of erythropoietin by the kidneys
■ Erythropoietin normally stimulates precursor cells in the bone marrow to produce RBCs
■ From decrease of functioning renal tubular cells
■ Decreased RBC life span
■ Increased hemolysis of RBCs
■ Frequent blood samplings
● Decreased iron stores
○ Sufficient iron stores are needed for erythropoiesis
○ Patients require iron supplementation
● Folic acid lost in dialysis
○ Folic acid is essential for RBC maturation
○ Folic acid is dialyzable because it is water soluble
○ Must be supplemented in the diet (folic acid 1 mg/day)
● Bleeding tendencies from GI tract
○ Defect in platelet function caused by impaired platelet aggregation and impaired release of platelet
factor III
○ Alterations in the coagulation system occur because of increased concentrations of both factor VII and
● Infection
o Cardiovascular system
○ Both a cause and consequence of CKS
■ Aggravated by sodium and water retention
■ Increased renin production may contribute
Lead to left ventricular hypertrophy and HF
HTN and DM are contributing risk factors for vascular complications
Long-standing HTN. Extracellular fluid volume overload, and anemia contribute to development of
left ventricular hypertrophy that may eventually lead to cardiomyopathy and HF
○ HTN can cause retinopathy, encephalopathy and nephropathy
Respiratory system
● Kussmaul respirations
○ With severe acidosis, the respiratory system attempts to compensate with Kussmaul respirations
which results in increased carbon dioxide removal by exhalation
● Dyspnea may occur with
○ Fluid overload
○ Pulmonary edema
○ Uremic pleuritic
○ Respiratory infections (pneumonia)
GI systems
● Every part of the GI system is affected
○ Cause: excessive urea
■ Stomatisis with ulcerations
■ Uremic fetor (urinous odor of breath)
■ Metallic taste in the mouth
■ Diabetic gastroparesis
● Can compound effects of malnutrition for patients with DM
■ GI bleeding
● Due to mucosal irritation and platelet defect
■ Constipation
● Due to ingestion of iron salts and/or calcium-containing phosphate binders.
● Limitations of fluid intake and physical inactivity can increase the risk of constipation.
○ Anorexia, nausea, vomiting may develop if CKD progresses to ESRD and is not treated with dialysis
Neurologic system
● CNS depression
○ Lethargy, apathy
○ Decreased ability to concentrate
○ Fatigue, irritability
○ Altered mental ability
○ Seizures & coma
■ May result from a rapidly increasing BUN
○ Hypertensive encephalopathy
(Seizures, coma, HTN encephalopathy -> not seen in early stages)
○ Peripheral neuropathy
Musculoskeletal system
● CKD mineral and bone disorder
○ Systemic disorder of mineral and bone metabolism caused by CKD
○ Less vitamin D is converted to its active form as the kidney deteriorates
Integumentary system
● Pruritus
○ Itching may be intense
○ Leads to bleeding or infection
small percentage of patients develop refractory pruritus that can have a devastating impact on their
well-being and quality of life
○ causes of pruritus
■ dry skin
■ calcium-phosphate deposition in the skin
■ sensory neuropathy
○ more prevalent in patients receiving dialysis than in earlier stages of CKD
● Uremic frost
○ Urea crystalizes on skin
○ Extremely rare condition
○ Usually seen only when BUN levels are extremely elevated (over 200 mg/dL)
o Reproductive system
● Infertility and decreased libido
○ Experienced by both sexes
● Sexual dysfunction
○ May also be caused by anemia, which causes fatigue
● Pregnancy poses significant risk to mother and infant
● Woman have decreased levels of estrogen, progesterone, and luteinizing hormone, which causes anovulation
and menstrual changes (usually amenorrhea)
● Men experience loss of testicular consistency, decreased testosterone levels and low sperm counts
● In addition, peripheral neuropathy can cause impotence in men and anorgasmia in women
● Psychological problems, physical stress and side effects of medications can cause changes in sexual function
● Sexual function may improve with maintenance dialysis and may become normal with successful
● Patients who become pregnant while receiving dialysis have been able to carry a fetus to term, but there is
significant risk to the mother and infant
● Pregnancy in patients with a kidney transplant is more common but there is still a considerable risk
o Psychological changes
● Personality and behavioral changes
● Emotional lability
● Withdrawal
○ Decreased ability to concentrate and slowed mental activity can give the appearance of dullness and
disinterest in the environment
● Depression
○ Changes in body image caused by edema, integumentary disturbances and access devices contribute
to depression and anxiety
○ Changes in lifestyle, occupation, family responsibilities and financial status
○ Grieving in loss of kidney function and independence.
● Fatigue and lethargy contribute to the feeling of illness
Diagnostic studies
o History and physical examination
o Dipstick evaluation of protein
● Proteinuria is usually the first indication of kidney damage
● Person with persistent proteinuria (1+ protein on standard dipstick, two or more times over a 3-month
period) should have further assessment of risk factors and a diagnostic workup with blood and urine tests
o Albuminuria is also evaluated which cannot be detected with a routine urinalysis
Patients with diabetes need to have examination of their urine for albuminuria is none is detected on routine
● Can detect RBCs, WBCs, protein, casts, and glucose
Renal ultrasound/biopsy
● Done to detect any obstructions and determine the size of the kidneys
● Kidney biopsy may be necessary to provide a definitive diagnosis
Albumin-to-creatinine ratio (first morning void)
● The two equations used most frequently to estimate GFR are the Cockcroft-Gault formula and the
Modification of Diet in Renal Disease (MDRD).
● MDRD is the preferred method.
o BP control is one of the most important therapeutic goals in management of
o Conservative therapy
● Correction of the ECF volume overload of deficit
● Nutritional therapy
● Erythropoietin therapy
● Calcium supplementation, phosphate binders
● Antihypertensive therapy
● Measures to lower potassium
● Adjustment of drug dosages to degree of renal function
o Drug therapy
● Hyperkalemia
○ Restriction of high-potassium foods and drugs
○ IV glucose and insulin
■ Acute hyperkalemia
○ IV 10 % calcium gluconate
■ Acute hyperkalemia
Sodium ploysturene sulfonate (Kayexalate)
■ Cation-exchange resin
■ Osmotic laxative action
■ Resin in bowel exchanges sodium ions for potassium ions
■ Used to lower potassium levels in stage 4 and can be administered in an outpatient basis
■ Tell the patient to expect some diarrhea because this preparation contains sorbitol, a sugar
alcohol that has an osmotic laxative action and ensures evacuation of the potassium from the
■ Never give to a patient with a hypoactive bowel (paralytic ileus) because fluid shifts could lead
to bowel necrosis
■ observe the patient for sodium and water retention
○ Dialysis may be needed
■ if changes appear in the ECG such as peaked T waves and widened QRS complexes dialysis
may be required to remove excess potassium
Treat HTN
○ Weight loss
○ Therapeutic lifestyle changes
○ Diet recommendations
○ Administration of antihypertensive meds
○ Limiting dietary phosphorus
○ Phosphate binders (Renagel)
■ Administer with meals
■ Usually given 8,12,4,8 (q4 hrs)
■ Constipation is a common side effect
○ Supplementing Vit D
○ Controlling hyperparathyroidism
Drug therapy complications
○ CKD causes decreased elimination that leads to an accumulation of drugs and potential for drug
○ Doses and frequency of administration are adjusted based on the severity of the kidney disease
○ Increased sensitivity may result as drug levels increase in the blood and tissues
○ Drug toxicity
■ Digoxin
■ Diabetic agents
● Metformin, glyburide
■ Antibiotics
● Vancomycin, gentamicin
■ Opioid medications
Dietary therapy
o Sodium restriction
● Diets vary from 2 to 4g/day
● Salt substitutes should be avoided; they contain K+, chloride
o Potassium restriction
● Limit: 2 to 3 g
● High-potassium foods should be avoided
o Phosphate restriction in ESRD
● Limit: 1 g/day
● Foods high in phosphate
○ Meat
○ Dairy products
● Most foods high in phosphate are also high in protein
○ Phosphate binders essentials since patients on dialysis are encouraged to eat a diet containing protein
■ Administer with meals
■ Calcium acetate (PhosLo)
■ Calcium carbonate (Caltrate)
● Bind phosphate in the bowel and then excreted
■ Sevelamer hydrochloride (Renagel)
● Lowers cholesterol and LDL levels
o Folic acid must be supplemented
o Iron supplementation
Nursing Assessment
o Complete hx of any existing kidney disease, family history
o Long-term health problems
o Drugs and herbal preparations
● Many drugs are potentially nephrotoxic, therefore ask the patient about current and past use of prescription
drugs, OTCs, and herbal preparations
● Medications of concerns are antacids, decongestants and antihistamines
● NSAIDs can contribute to the development of AKI and progression of CKD, especially when taken in higher
doses than recommended
o Dietary habits
● Discuss problems regarding intake
● Measure height and weight
● Evaluate any weight changes
o Support systems
Movement of fluid/molecules across a semipermeable membrane from one compartment to another
Used to correct fluid & electrolyte imbalances & to remove waste products in kidney failure
Can be used to treat drug overdoses
Begun when patient’s uremia can no longer be adequately treated conservatively
Initiated when GFR <15 mL/min/1.73 m2
3 x a week
Hemodialysis (HD)
● In HD an artificial membrane (usually made of cellulose-based or synthetic materials) is used as the
semipermeable membrane & is in contact with the patient’s blood.
● Vascular access sites (obtaining one is one of the most difficult problems)
● Subcutaneous arteriovenous fistulas (AVF) - created in the forearm or upper arm with an anastomosis
between an artery & a vein (usually cephalic/basilic)
■ Allows arterial blood to flow through the vein
■ Vein becomes “arterialized”, increasing in size & developing thicker walls
■ Maturation may take 6 weeks-months
■ AVF should be placed 3 months before need to initiate HD
■ Preferred access for HD
■ Normal -> feel a thrill, hear a bruit
■ Difficult to create in patients with Hx of severe PAD, prolonged IV drug use, & obese women
● Arteriovenous grafts (AVGs) are made of synthetic materials (Teflon) & form a “bridge” between the
arterial & venous blood supplies
■ Placed under the skin & are surgically anastomosed between an artery (usually brachial) & a
vein (usually antecubital)
■ More likely to become infected & have a tendency to be thrombogenic
● Temporary vascular access - for immediate access, percutaneous cannulation of the internal
jugular/femoral vein is performed
● Management
● Assess:
○ fluid status (weight, BP, peripheral edema, lung & heart sounds)
○ condition of vascular access
○ temperature
■ During dialysis
● Take vital signs every 30-60 mins
■ Post-dialysis
● Difference between last postdialysis weight & present predialysis weight determines
ultrafiltration/the amount of weight (from fluid) to be removed
Question: A patient undergoes peritoneal dialysis exchanges several times each day. What should the nurse plan to
increase in the patient’s diet?
a. Fat
b. Protein
c. Calories
d. Carbohydrates
Recommended protein intake is at least 1.2 g/kg of ideal body weight per day
● Hypotension
○ Results primarily from:
■ rapid removal of vascular volume (hypovolemia)
■ decreased cardiac output
■ decreased systemic intravascular resistance
● Muscle cramps
○ Factors associated include:
■ Hypotension
■ Hypovolemia
■ High ultrafiltration rate (large interdialytic weight gain)
■ Low-sodium dialysis solution
● Loss of blood
○ May result from:
■ not blood not completely rinsed from the dialyzer
■ accidental separation of blood tubing
■ dialysis membrane rupture
■ bleeding after the removal of needles at the end of HD
● Hepatitis
○ Hepatitis C virus (HCV) is responsible for the majority of cases of hepatitis in dialysis recipients
Peritoneal Dialysis (PD)
In PD the peritoneal membrane acts as the semipermeable membrane.
● Peritoneal access is obtained by inserting a catheter through anterior abdominal wall
● technique varies, usually done via surgery
● Pre-procedure: empty bladder & bowel, weigh patient, obtain a signed consent form
● Solutions:
● Three phases of the PD cycle
Inflow (fill) - a prescribed amount of solution (usually 2L) is infused through catheter over about
10 mins; slow flow rate if patient is in pain
■ Dwell (equilibration) - diffusion & osmosis occur between the patient’s blood & peritoneal
cavity; 20-30 mins… or up to 8+ hrs depending on method
■ Drain - 15-30 mins; gently massaging the abdomen/changing position; another infusion of 2L of
● Ultrafiltration (fluid removal) during PD depends on osmotic forces, with dextrose being the most
commonly used osmotic agent in PD solutions
● Available in 1-/2-L plastic bags with glucose concentrations of 1.5%, 2.5%, & 4.5%
● Electrolyte composition similar to that of plasma
● Solution warmed to body temperature
● PD Systems
● Automated Peritoneal Dialysis (APD)
■ Most popular form of PD
■ Allows patients to do dialysis while they sleep
■ Cycler (automated device) is used to deliver the dialysate for APD
■ The machine cycles 4+ exchanges per night with 1-2 hours per exchange
● Continuous ambulatory peritoneal dialysis (CAPD)
■ Performed every few hours during the day
■ May perform an exchange of 2 L of peritoneal dialysate 4x daily, with dwell times averaging 4
■ Patient instills 2-3 L of dialysate into the peritoneal cavity through a disposable administration
● PD Complications
● Exit site infection
■ Most commonly caused by Staph auerus/Staph epidermidis (from skin flora) -> s/s = redness at
site, tenderness, & drainage
● Peritonitis
■ Most frequently occurs because of improper technique when connections for exchanges are
■ Usually caused by Staph auereus/Staph epidermidis
■ s/s
● abdominal pain
● rebound tenderness
● cloudy peritoneal effluent wit a WBC > 100 cells/µL (> 50% neutrophils) or
demonstration of bacteria in the peritoneal effluent by Gram stain/culture.
● GI s/s
○ Diarrhea
○ Vomiting
○ Abdominal distension
○ Hyperactive bowel sounds
○ Fever may/may not be present
■ Confirm with culture, gram stain, & WBC differential of peritoneal effluent
● Hernias
Can develop in multiparous women & older men because of increased intraabdominal pressure
secondary to the dialysate volume
Lower back problems
■ Lumbosacral curvature is increased by intraperitoneal infusion of dialysate -> treatment =
orthopedic binders & regular exercise program
Pulmonary complications
■ Atelectasis, pneumonia, & bronchitis may occur from repeated upward displacement of the
diaphragm, resulting in decreased lung expansion -> treatment = deep-breathing, elevate head
of bed to prevent these problems
Protein loss
■ Amount of loss is usually about 0.5 g/L of dialysate drainage -> can be as high as 10-20 g/day
Benign Prostate Hyperplasia (BPH)
● Enlargement of prostate gland leading to disruption of urine outflow from bladder-urethra
● Etiology of BPH is not completely understood
● Hormonal changes associated with aging are believed to be contributing factors
○ Dihydroxytestosterone (DHT) - sex hormone that stimulates prostate cell growth
■ Excess amount can cause overgrowth of prostate tissue
■ As men age, testosterone decreases, but dihydroxytestosterone continues to produce
○ Estrogen
■ As men age the amount of active testosterone in the blood decreases, leaving a higher
proportion of estrogen -> promotes prostate cell growth
● BPH usually develops in the inner part of the prostate
○ Gradually compresses on the urethra, leading to partial or complete obstruction
■ Compression leads to the development of clinical manifestations
■ Size of prostate does not equal the severity of manifestations or the degree of obstruction
■ Location of enlargement is most significant in the development of obstructive symptoms
● Almost 50% will have lower urinary tract symptoms (LUTS)
○ Difficulty starting a urine stream, decreased flow of urine, urinary frequency
● Risk factors for BPH:
○ Aging
○ Obesity (esp. Waist circumference)
○ Lack of physical activity
○ Alcohol consumption
○ Erectile dysfunction
○ Smoking
○ Diabetes
● Goals:
○ Restore bladder drainage
○ Relieve symptoms
○ prevent/treat complications
● Active surveillance -> annual PSA & DRE
● Based on
● How bothersome are the symptoms
● Presence of complications
● NOT based on the size of the prostate
● Drug therapy
● 5⍺-reductase inhibitors
■ Finasteride (Proscar)
■ Dutasteride (Avodart)
■ Dutasteride + Tamsulosin (Jalyn)
● ⍺-Adrenergic receptor blockers
■ Silodosin (Rapaflo)
■ Alfuzosin (Uroxatral)
■ Doxazosin (Cardura)
■ Prazosin (Minipress)
■ Terazosin
■ Tamsulosin (Flomax)
● Minimally Invasive Therapy
● Transurethral Microwave Thermotherapy (TUMT)
● Transurethral Needle Ablation (TUNA)
● Laser Prostatectomy
● Transurethral Electrovaporization of the Prostate (TUVP)
● Invasive Therapy (Surgery)
● Transurethral Resection (TURP)
■ “Gold standard” surgical treatment for obstructing BPH but requires a hospital stay (costly)
■ Used less frequently due to development of less invasive technologies
■ Low risk, but MUST watch for:
● TUR/TURP syndrome (temporary)
○ s/s -> N/V, confusion, bradycardia, HTN
○ Results from hyponatremia due to longer operative times & prolonged
intraoperative bladder irrigation
● Bleeding & clot retention (post-op)
○ Patients on aspirin, warfarin, & other anticoagulants must D/C several days
before surgery
■ BPH medications also stop after this procedure
■ Post-op care:
● Assess for complications:
○ Hemorrhage
○ Bladder spasms
○ Urinary incontinence
○ Infection
○ Postoperative bladder irrigation
○ Manually on an intermittent basis
○ Continuous bladder irrigation (CBI)
■ Remove blood clots
■ Ensure drainage of urine
■ Use aseptic technique
■ Transurethral Incision of the Prostate (TUIP)
Open prostatectomy
Bladder cancer risk factors
● Risk factors
Ages 60-70 (most common)
Three times more common in men
Cigarette smoking
Exposure to dyes in the rubber and other industries
Chronic abuse of phenacetin-containing analgesics
Women treated with radiation for cervical cancer
Patients who received cyclophosphamide
Patients who take the DM drug pioglitazone
Chronic, recurrent calculi
Chronic lower UTIs
Patients who have indwelling catheters for long periods
Kidney transplantation
The best tx option available to patients with ESKD
Kidney transplantation reverses many of the pathophysiological changes associated with renal failure
Eliminates the dependence on dialysis and the accompanying dietary and lifestyle restrictions
Transplantation is less expensive than dialysis after the first year
Recipient selection
● Some transplant programs excludes patients who are morbidly obese and who continue to smoke
● Careful evaluation is completed to minimize complications after transplantation
● Contraindications
○ Disseminated malignancies
○ Refractory or untreated cardiac disease
○ Chronic respiratory failure
○ Extensive vascular disease
○ Chronic infection
○ Unresolved psychosocial disorders
■ Nonadherence to medical regimens
■ Alcoholism
■ Drug addiction
Donor sources
● Kidneys may be obtained from
○ Compatible blood-type deceased donors
○ Blood relatives
○ Emotionally related living donors
○ Altruistic living donors who are known or unknown to recipient
○ Paired organ donation
● Live donors
○ Crossmatched are done at time of evaluation and a week before the transplant to ensure that no
antibodies to the donor are present
○ Advantages include
■ a better patients and graft survival rate
■ Immediate organ availability
■ Immediate function because of minimal cold time
■ opportunity to have the recipient in the best possible medical condition
○ Potential donor sees a nephrologist for a complete history, physical exam, and lab + diagnostic studies
○ Transplant psychologist or social worker determines if the patient is emotionally stable and able to deal
with issues r/t organ donation
Deceased donors
○ Must have effective CV functions and be supported on a ventilator to preserve organs.
○ Must be free of
■ active IV drug abuse
■ Severe HTN
■ Long standing DM
■ Malignancies
■ Sepsis
■ Communicable disease
○ Kidneys can be served for up to 72 hours
■ Most surgeons prefer to transplant before the cold time (time the kidney is outside the body)
reaches 24 hours
Nursing Management
● Pre-op care
○ Emotional and physical preparation
○ Review of operative procedure and what can be expected during post-op recovery
○ Stress that there is a chance the kidney might not function immediately and dialysis may be needed
○ Review the need for immunosuppressive drugs and measures to prevent infection
○ ECG, chest x-ray and lab studies are ordered
○ Patency of dialysis access should be maintained
● Post-op care
○ Donor
■ Monitor renal function
■ Monitor hematocrit
■ Acknowledge the gift that they gave
○ Recipient
■ Maintenance of fluid and electrolyte balance
■ Monitor urine output
■ Monitor central venous pressure readings
■ Acute tubular necrosis
● May occur from prolonged cold times
● Dialysis is required
● Can last from days to weeks
■ Maintain catheter patency
■ Discharge planning and teaching
● Complications of transplantations
○ Rejection
■ Hyperacute
■ Acute
■ Chronic
● Should be put on transplant list in hope to be re-transplanted before starting dialysis
Cardiovascular disease
■ Teach patient to control risk factors such as
● Elevated cholesterol
● Elevated triglycerides
● Elevated BG
● Weight gain
■ Adherence to prescribed antihypertensive regimen is essential
■ Regular screening for cancer is important part of recipients preventive care.
■ Advise patient to avoid sun exposure by using protective clothing and sunscreens
Recurrence of original kidney disease
■ Patients must be advised before the transplantation if they have
● Glomerulonephritis
● IgA nephropathy
● Diabetic nephropathy
● Focal segmental sclerosis
Corticosteroid-related complications
■ Vigilant monitoring for side effects of corticosteroids and early tx are essential
UTI including manifestations and medications
Fungal and parasitic infections may also cause UTIs but they are uncommon causes
○ Defense mechanism alterations
■ Acidic pH less than 6
■ High urea concentration
■ Abundant glycoproteins
Risk factors
○ Immunosuppressed
○ Diabetic
○ Kidney problems
○ Have undergone multiple antibiotic courses
○ Have traveled to developing countries
○ Predisposing factors
■ Factors increasing urinary stasis
○ BPH, tumor, neurogenic bladder
■ Foreign bodies
○ Catheters, calculi, urinary tract instrumentation
■ Anatomic factors
○ Obesity, fistula, congenital defects, shorter female urethra
■ Compromising immune response factors
○ HIV, aging
■ Functional disorders
○ Constipation, voiding dysfunction
■ Other factors
○ Pregnancy, menopause, multiple sex partners, use of spermicidal agents or
contraceptive diaphragm, poor personal hygiene, habitual delay of urination
Upper versus lower
○ Upper urinary tract
■ Renal parenchyma, pelvis and ureters
■ Typically causes fever, chills, flank pain
■ Example
● Pyelonephritis
○ Inflammation of renal parenchyma and collecting system
Lower urinary tract
■ Usually no systemic manifestations
■ Examples
● Cystitis
○ Inflammation of the bladder
● Urethritis
○ Inflammation of urethra
■ Manifestations
● Emptying symptoms
○ Hesitancy
○ Intermittency
○ Post void dribbling
○ Urinary retention or incomplete emptying
○ Dysuria
○ Hematuria
● Storage symptoms
○ Urinary frequency
○ Urgency
○ Incontinence
○ Nocturia
○ Nocturnal enuresis
Drug therapy
○ Antibiotics
■ Ciprofloxacin
■ trimethoprim/sulfamethoxazole (Bactrim, Septra)
● Inexpensive
● Taken twice daily
● May be E.coli resistant (disadvantage)
■ Trimethoprim alone in patients with sulfa allergy
■ Nitrofurantoin (Macrodantin, Macrobid)
● Usually taken 3-4 times a day
● Macrobid is a long acting preparation given twice daily
● Avoid sunlight
● Notify physician if any adverse effects develop
○ Fever, chills, cough, chest pain, dyspnea, rash or numbness of fingers or toes.
■ Fosfomycin (Monurol)
○ Antifungals
○ Urinary analgesic
● Used in combination with antibiotics
● Provides soothing effect on urinary tract mucosa
● Strains urine reddish orange
○ Can be mistaken for blood and may stain clothing
Urinary Tract Calculi
Etiology & pathophysiology
● Stone formation
○ Mucoprotein forms matrix
○ Affected by
■ Urinary pH (alkaline)
● The higher the pH (alkaline), the less soluble are calcium & phosphate
● The lower the pH (acidic), the less soluble are uric acid & cystine
■ Solute load
● When a substance is not very soluble in fluid, it is more likely to precipitate out of
■ Inhibitors in urine
○ Other factors
■ Obstruction with urinary stasis
● Urinary stasis & UTI with urea-splitting bacteria (ex - Proteus, Klebsiella,
Pseudomonas, & some Staph. species) can cause the urine to become alkaline &
contribute to the formation of struvite stones
● Infected stones (entrapped in the kidney)
○ may assume a staghorn configuration as the stone branches to occupy a large
portion of the collecting system
○ Can lead to
■ renal infection
■ hydronephrosis
■ Loss of kidney function
■ Genetics
● Cystinuria, an autosomal recessive disorder, is characterized by a marked increased
excretion of cystine
● Clinical Manifestations
○ Renal colic
■ Sharp, sudden severe pain that results from the stretching, dilation, & spasm of the ureter in
response to the obstructing stone
■ Flank area, back, or lower abdomen
○ Common sites of obstruction
■ Ureteropelvic junction (UPJ)
● Dull pain in costovertebral flank
● Renal colic
■ Ureterovesical junction (UVJ)
● Interprofessional Care
○ Management of acute attack
■ Administer opioids to relieve colic pain
■ Medications = Tamsulosin (Flomax)/ Terazosin
Evaluation of the cause of stone formation
■ Family Hx
■ Geographic location
■ Nutritional assessment
● Intake of vitamins A & D
■ Activity pattern
■ Prolonged illness, disease, surgery
Nursing Implementation
○ Teach methods to prevent recurrence
■ Lifestyle & diet changes
● Adequate fluid intake
○ To produce approx. 2 L of urine per day
○ Moderately active, ambulatory persons should drink about 3 L/day
○ Fluid intake will need to be higher in the active person who works
outdoors/who regularly engages in athletic activities
● Dietary restriction
○ Avoid purines - may be helpful for patients at risk for developing uric acid
Points to Remember
● Use the PPT slides and lecture notes as guidelines for study purpose.
● Read your Lewis textbook to focus on details.
● Arrive in class ready to take the exam at least 10 minutes prior to exam time.
● Know the last 4 digits of your student ID.
Best of Luck!