Acute Renal Failure:

Pathophysiology /Etiology - Potential causes of the patients problem

Acute renal failure is a sudden loss of kidney function caused by damage to the tubules, damage to the
glomeruli, or the failure of renal circulation.

This damage is often reversible, with recovery occurring in a few days to weeks.

Ischemia is the primary cause of acute renal failure. When occurring for longer than two hours, the
tubules may suffer irreversible damage.

Three categories summarize acute renal failure. These are identified by location. These are:

Prerenal, Intra renal, and Postrenal.

Prerenal accounts for 55% of all renal failure. This is caused by decreased blood flow to the kidneys. It
is reversible when recognized in a timely fashion, and treated quickly. Causes of Prerenal failure are
severe dehydration, circulatory collapse, shock, hypovolemia, or diuretic therapy. Other causes include
Shock, Heart Failure, Pulmonary Embolism, Anaphylaxis, Sepsis, and pericardial tamponade.

Intrarenal is typically caused by ischemia, a disease process, or toxic conditions such as acute
glomerulonephritits, vascular disorders, severe infection, or toxic agents. Itrogenic causes include
antibiotics and contrast dyes. Listed also is acute interstitial nephritis, Exposure to nephrotoxins, acute
glomerular nephritis, vasculitis, acute tubular necrosis, renal artery or vein stenosis renal artery or vein
thrombosis, and formation of crystals or precipitates in the nephron tubules.

Postrenal is caused by obstructions in the flow from the kidneys. Such restrictions and obstructions may
be caused by BPH, tumors, or renal and urinary calculi.

Clinical Manifestations:

There are three or four defined phases to the manifestations of renal failure depending on the text.
Hogan lists three phases; the initiation phase, maintenance phase, and the recovery phase. Ignatavicius
list four; Onset, Oliguric, Diuretic, and Recovery phase. The difference being, Hogan appears to
incorporate the Diuretic phase as the onset or part of to the recovery phase.

The Onset phase begins with the precipitating event lasting hours to days. During this phase there is a
gradual accumulation of nitrogenous waste. This phase leads to the Oliguric phase.

In the Oliguric phase urine output decreases to less than 400 mL/24hours.

Prior to the recovery phase, a Diuretic phase occurs. In this phase urine output rapidly increases.
Output can exceed 10 L/day.
In the recovery phase urine output returns to normal, but complete recovery may take upto 12 months.
A patient in this phase may have lower energy levels and less stamina than before the illness.

Symptoms include Muscle weakness, Nausea, Vomiting, and diarrhea. Neurologic symptoms present as
confusion, agitiation, seizures, disorientation, and coma.

Laboratory and Diagnostic test will show hyperkalemia, hyperphosphatemia, hypocalcemia, metabolic
acidosis, azotemia, anemia, elevated creatinine and BUN levels, proteinuria, and urine at a specific
gravity equal to plasma. Urine analysis will further reveal casts, RBC, WBC, and renal tubular epithelial
cells.

Nursing Care:

Priority nursing interventions are based around excess fluid volume, risk for infection, imbalanced
nutrition, less than body requirements, and deficient knowledge.

The nurse should monitor I & Os.

Observations should look for olguria followed by a period of polyuria.

Daily weight measurements should be taken. Monitor for acidosis and hyperkalemia as signs of
electrolyte imbalance.

Discuss with the patient their concerns over the disorder.

Monitor nutritional requirements. Have patient follow a diet high in carbohydrates with moderate
protein restriction and potassium restrictions.

With start of diuresis lab results should indicate a return of creatinine, phosphorus, BUN and potassium
to normal.

Avoid nephrotoxic drugs: plantinoid chemotherapy agents, NSAID, Contrast media, and aminoglycoside
antibiotics.

Use of volume expanders to restore renal perfusion. Use of Dopamine intravenously to increase renal
blood flow.

Loop diuretics can be used to reduce toxic concentrations in the nephrons.

Ace inhibitors should be subscribed to control hypertension.

Antacids will help reduce gastric ulcers.

Medicate with sodium polystyrene sulfate to reduce serum potassium levels.

Use sodium bicarbonate to treat acidosis.

Safety Issues:

Dietary and fluid restrictions should be followed.

Discuss with the patient signs of complications such as Excess fluid volume, CHF, and hyperkalemia.

Continue to monitor blood pressure, pulse rate, Urinary output, and weight gains or losses.

Patient should avoid any nephrotoxic drugs, NSAIDS, contrast medias, heavy metal drugs, and should
consult their doctor prior to taking OTCs/

Renal recovery can take upto 12 months. Nephrons are vulnerable to further damage from
nephrotoxins until fully healed.

Patient Outcomes:

The patient will verbalize understanding of dietary and fluid restrictions.

The patient will verbalize the need to avoid nephrotoxic substances.

The patient will identify signs of infection, and know when to consult a physician.

The patient will be able to demonstrate the ability to monitor blood pressure, pulse, and urine output.

The patient will maintain their weights and vital signs within normal ranges.

The patient will have renal function restored within 12 months.

Teamwork and Collaboration:

Consultation should exist between the patient, nursing, dietary, the patient’s physician, pharmacy, and
home care.
Resources:

Ignatavicius, Donna D.. Medical-Surgical Nursing: Patient-Centered Collaborative Care, 6th Edition. W.B.
Saunders Company

Hogan, Mary Ann Medical Surgical Nursing: Reviews and Rationals, 2 nd Edition. Prentice Hall Nursing.

Chronic Renal Failure:

Pathophysiology:

Chronic renal failure is characterized by a glomular filtration rate less than 20% of normal function.
There are five stages of chronic renal failure, with the last stage ending fatally with uremia. Chronic
renal failure differs from acute, in that it is slow, progressive loss.

The common causes of chronic renal failure are hypertension, systemic lupis erthematosus, diabetic
neuropathy, glomerulonephritis, and cystic kidney disease.

With destruction of over 90% of the neprhons, BUN and creatinine Clearance rises. With this urine
specific gravity also becomes fixed at 1.010.

End stage renal failure is the final stage of chronic renal failure, and is associated with Uremia, urine in
the blood.

With the loss of erythropoietin chronic anemia and fatigue occur.

Inadequate clearance of fluids and electrolytes leads to fluid and sodium retention. Hyperkalemia,
hypermagnesemia, hyperphosphatemia, azotemia, and hypocalcemia can occur as a result of this
imbalance. When hypocalcemia occurs there is an increase in parathyroid secretion and calcium loss
from bones.

Clinical Manifestations:

CRF has early manifestations as nausea, apathy, weakness, and fatigue.

Late stages will manifest with frequent vomiting, increasing weakness, confusion, and lethargy.

The patient may experience parethesia and sensory loss.

Seizures, hallucinations, irritability, anxiety, and coma can occur in late stages.

Kussmaul pattern breathing in late stages is followed by coma.

Skin becomes yellow, pale, and dry. Uremic frost and itching occurs as the result of metabolic wastes on
the skin.

Lab Values:

Specific gravity fixed at 1.010

Elevated creatinine and BUN

Decreased creatinine clearance.

Abnormal electrolyte values.

Moderate anemia.

Decreased platelets.

Ultrasonography can confirm decreased renal size.

Biopsy of renal tissue can confirm if damage was caused by cancer.

Nursing Care:

Impaired tissue perfusion, imbalanced nutrition, risk for infection, Excess fluid volume, activity
intolerance, and disturbed body image are all areas the nurse has to address.

A diet will be provided that is low in protein with supplemental amino acids. Fluids will be restricted.

Restrictions will be made to sodium & potassium. Calcium and bicarbonates will need to be replaced.

Monitor and treat for hypertension and heart failure.

Prepare the client for dialysis; or if eligible prepare the client for kidney transplant.

Medications should be administered with caution as they cannot be excreted through the kidneys.

Monitor I &Os

Monitor Laboratory results for serum creatinine, BUN, pH, CBC, and electrolytes.

Provide relief for nausea and vomiting.

Monitor for infection.

Help the patient develop coping strategies for dealing with the diagnosis and complications.

Teach strategies to avoid thirst: Sugarless hard candy, ice chips, squirt bottles.
Medication therapy will be similar to that of acute renal failure discussed previously.

Patient Safety:

Monitor weight, vital signs and urine output.

Monitor for symptoms of uremia

Avoid nephrotoxic medications

Monitor for infection

Monitor for anxiety

Assess for early signs of pulmonary edema.

Assess for fluid overload.

Patient Outcomes:

The patient will be able to show an understanding of the dietary and fluid restrictions.

The patient will be able to show anxiety management towards their diagnosis.

The patient will show understanding for the need to avoid nephrotoxic substances.

The patient will be able to discuss the signs of infection and know when to talk to their physician.

The patient will take medications as ordered.

Teamwork and Collaboration:

Consultation should exist between the patient, nursing, dietary, the patient’s physician, pharmacy, and
home care.

Resources:

Ignatavicius, Donna D.. Medical-Surgical Nursing: Patient-Centered Collaborative Care, 6th Edition. W.B.
Saunders Company

Hogan, Mary Ann Medical Surgical Nursing: Reviews and Rationals, 2nd Edition. Prentice Hall Nursing.
Thyroid/parathyroid disorders:
Pathogenisis:

Hyperthyroidism is the excessive secretion of thyroid hormone from the thyroid gland. It can be caused
by the excess secretion of TSH from the pituitary gland, thyroiditis, autoimmune reaction, or tumors.

Hyperthyroidism known more specifically as Grave’s disease is the most common of the thyroid
disorders. Graves disease occurs more often in women between the ages of twenty and forty at a rate
of five times. Grave’s disease is caused by an autoimmune disorder that causes an oversecretion of
thyroid hormone by the thyroid gland. Iodine insufficiency is highly associated with Grave’s disease.

Manifestations of hyperthyroidism:

Manifestations range from minor to extremely severe based on the level of hormones secreted.

Thyroid crisis also known as thyroid storm is a life threatening emergency in the most extreme cases. It
is a significant risk in people who have long term untreated hyperthyroidism. Manifestations of Thyroid
storm include: a temperature greater than 102 F, tachycardia, abdominal pain, systolic hypertension,
nausea, diarrhea, vomiting, tremors, confusion, and seizures.

Nursing Care:

Primary nursing care of a patient with hyperthyroidism is associated around treatments.

The nurse will be concerned about cardiac output, ineffective airway clearance, imbalanced nutrition,
hyperthermia, and disturbed sleep.

In treating hyperthyroidism, Iodine 131 is used.

It is not to be used with pregnant women.

Patient should drink fluids through a straw.

The nurse will monitor vitals and weight.

Another treatment method is a thyroidectomy.

Preoperative the nurse will teach the patient deep breathing exercises and methods to cough.

Postoperatively, the nurse will provide comfort through analgesics and positioning.

The nurse will monitor for hemorrhage, and promote a patent airway.

The nurse will prevent tetany by monitoring Calcium levels for hypocalcemia. Hypocalcemia
being detectable with the Chvostek’s and Trousseau signs.

The nurse will maintain a patent IV site.

 The nurse will monitor for laryngeal nerve damage by asking the patient to speak in a loud tone
of voice.

Patient teachings will include:

Regular eye exams, call a physician if any changes in vision occurs. Protect the eyes with tinted
glasses.

Moisten eyes frequently with artificial tears.

Sooth dry eye with cool moisten towels.

Elevate the head of the bed to lessen pressure on the optic nerve.

Use cool compresses for dry eye irritation

Elevating the head of the bed will put less pressure on the optic nerve.

Assist the client to understand the surgical procedure and wound care.

Assist the patient with lifestyle changes and coping with self-image changes.

Safety for Hyperthyroidism:

The patient’s VS should be monitored regularly

Looking for signs of thyroid sign are imperative.

Patient outcomes:

The client will verbalize an understanding of their medication requirements.

The patient will be able to perform eye and wound care.

The patient will recognize symptoms they should report to their physician.

The patient will show how to support the neck post-op.

The patient will be able to show acceptance of lifestyle-changes and perform normal social interactions.
Pathogenesis hypothyroidism

Hypothyroidism occurs when there is an insufficient amount of thyroid hormone secreted by the thyroid
gland. This decreases metabolic rate and heat production.

99% of the cases of hypothyroidism are Primary hypothyroidism. This disease is five to seven times
more common in women. 50% of the cases diagnosed indicate anti-body mediated destruction , or cell
mediated destruction of the thyroid gland.

Other pathos for this disease in include thyroiditis, iatrogenic infections, iodine deficiency, subacute
postpartum, congenital or idiopathic.

Secondary hypothyroidism is a result of insufficient secretion of TSH from the pituitary gland, or
associated with TRH deficiency of the hypothalamus.

Clinical manifestations of hypothyroidism:

Enlarged thyroid gland that forms a goiter.

Symptoms that include: lethargy, periorbital edema, diminished reflexes, bradycardia, dysrithmias,
hypotension, reproductive problems, dry hair, dry skin, and signs of slowed metabolism.

Nursing care for hypothyroidism:

The nurse should assess for myxedema.

Laboratory test should be monitored for decreased T4 and free T4 levels.

Normal T3 levels should be monitored with TSH levels.

Medications should be sought that will replace T4 that has not been generated from T3.

The nurse should monitor for Decreased cardiac output, poor nutrition, constipation, impaired skin
integrity, activity intolerance, hypothermia, sexual dysfunction, and disturbed body image.

Medication for hypothyroidism should be given an hour before the first meal of the day or two hours
after.

Provided blankets to the patient to help maintain a comfortable temperature.

Activities should include rest periods to minimize activity intolerance.

The patient will be advised to increase fluid intake to at least 2000 mL and diet should focus on high
fiber food.
Safety issues for hypothyroidism:

Myxedema as characterized by: non-pitting edema, puffy face and togue, severe metabolic disorders,
hypothermia, cardiac collapse, and coma.

Hold hypothyroid medication if HR is greater than 100.

Be aware of sudden weight gains or losses, heat or cold intolerances, and chest pain.

Potential outcomes of hypothyroidism:

The patient will be able to self-administer medications.

The patient’s weight has stabilized.

ADLs are tolerated with no signs of abnormal fatigue.

The patient does not have discomfort or SOB during ADLs.

The patient has normal sleep patterns.

The patient’s skin is elastic and intact.

Teamwork and Collaboration for thyroid disorders:

Consultation should exist between the patient, nursing, dietary, the patient’s physician, pharmacy, and
home care.

Resources:

Ignatavicius, Donna D.. Medical-Surgical Nursing: Patient-Centered Collaborative Care, 6th Edition. W.B.
Saunders Company

Hogan, Mary Ann Medical Surgical Nursing: Reviews and Rationals, 2nd Edition. Prentice Hall Nursing.

Parathyroid disorders:
Pathogenesis:

Hyperparathyroidism is associated wit increased parathyroid secretions from the parathyroid gland.
Primary hyperparathyroidism is the result of hyperplasia, or a tumor of one of the parathyroid glands.
This disorder will cause increased absorption of calcium into the GI tract.
Secondary hyperparathyroidism is the result of gland enlargement from chronic hypercalcemia in the
presence of elevated PTH.

Tertiary hyperparathyroidism is a result of enlarged parathyroid glands that do not respond to changes
in serum calcium levels. Tertiary hyperparathyroidism often occurs with chronic renal failure.

In hyperparathyroidism there is an increased rate of reabsorption of calcium and increased phosphate

levels. This leads to hypercalcemia and hypophosphatemia. There is an increased excretion of
bicarbonate from the kidneys, and a decrease in acid excretion. This leads to metabolic acidosis and
hypokalemia. Because of the increased rate of calcium and phosphorus release, bones begin
decalcification. Free calcium in the system becomes deposited into soft tissues, can form renal calculi,
alter neurological function, Alter GI function, and can yield constipation, abdominal pain, anorexia, and
alter cardiovascular funcition.

Hypoparathyroidism is the result of hypocalcemia after the surgical removal of a parathyroid gland. This
results in abnormally low PTH levels. This raises the excitability of nerve and muscle fibers casuig them
to be easily stimulated. Life threatening tetany is the result.

Clinical manifestations:

Hyperparathyroidism manifest as polyuria, renal calculi, anorexia, constipation, vomiting, and

abdominal pain. Bone pain results from decalcification and pathologic fractures. Muscle weakness and
atrophy also occurs. Laboratory test will reveal elevated serum levels of total calcium, increased PTH, &
decreased phosphate. Bone loss and degradation may be viewable on X-rays and CT scans.

Hypoparathyroidism manifests similar GI issues, but neurologically, hypocalcemia results in anxiety,

headaches, parethesias, and neuromuscular disorders. Tremors, muscles spasms can occur. A patient
may have difficulty swallowing, have a hoarse voice, and tightness in the throat.

Nursing care of parathyroidism:

Both disorders require a nurse to assess risk for injury and knowledge deficiencies regarding the
disorder and treatment.

Hyperparathyroidism further evaluates pain, impaired motility, altered urinary elimination, and
constipation.

Hypothyroidism focuses more on the sensations of anxiety.

In hyperparathyroidism, the nurse will promote comfort and safety when trying to ambulate the
patient.

Urine will be strained for the presence of renal calculi.

An increased fluid diet will be given as tolerated. Meals will consist of a high fiber diet.

The patient will be weighed daily.

The patient will be given analgesics to help with the pain. Diureticsw will be administered to help
remove excess calcium in the serum; and biphosphinates may be administered to inhibit bone
reabsorption.

In hypoparathyroidism the nurse will provide supplemental calcium and Vitamin D.

The nurse will encourage increased motility as tolerated with assistance if required.

The nurse will discuss anxiety issues with the patient, and help the patient find ways to deal with the
anxiety.

Patient outcomes:

The patient will verbalize an understanding of medications and supplements.

The patient will recognize symptoms and report them to the physician.

The patient will express an understanding of dietary restrictions and modifications.

Additionally in hyperparathyroidism, the patient will be able to discuss pain control.

In hypoparathyroidism the patient additionally will discuss the necessity of a med-alert ID bracelet and
demonstrate meal planning.

Teamwork and Collaboration for parathyroid disorders:

Consultation should exist between the patient, nursing, dietary, the patient’s physician, pharmacy,
wound care, radiology, and home care.

Resources:

Ignatavicius, Donna D.. Medical-Surgical Nursing: Patient-Centered Collaborative Care, 6th Edition. W.B.
Saunders Company

Hogan, Mary Ann Medical Surgical Nursing: Reviews and Rationals, 2nd Edition. Prentice Hall Nursing.