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The nephron is the functional unit of the kidney. Each kidney contains approximately 1 million nephrons.  Each nephron is composed of the glomerulus, Bowman's capsule, and a tubular system.

The tubular system consists of the proximal convoluted tubule, loop of Henle, distal convoluted tubule, and collecting tubules.

The glomerulus, Bowman's capsule, proximal tubule, and distal tubule are located in the cortex of the kidney.

The loop of Henle and collecting tubules are located in the medulla. Several collecting tubules join to form a single collecting duct. The collecting ducts eventually merge into a pyramid that empties via the papilla into a minor calyx.

Selective Filtration

Proximal tubule – Reabsorption of 80% of electrolytes and H2O, all glucose and amino acids, HCO3; secreation of H+ and creatinine

c

Loop of Henle– Ascending limb - Reabsorption of Na+ and Cl- ; descending loop – reabsorption of H2O; conceration of filtrate

Distal tubule – Secretion of K+, H+, ammonia; reabsorption of H2O (reulated by ADH); reabsorption of HCO2; regulation of Ca2+ and PO2/4 by parathyroid hormone, regulation of Na+ and K+ by aldosterone

c

Collecting duct -  Reaabsorption of water (ADH required)

What are the age related changes in the renal system?

Anatomic changes in the aging kidney include a 20% to 30% decrease in size and weight between ages 30 and 90 years. By the seventh decade of life, 30% to 50% of glomeruli have lost their function.Atherosclerosis accelerates the decrease of renal size with age. Despite these changes, older individuals maintain body fluid homeostasis unless they encounter diseases or other physiologic stressors.5

Physiologic changes in the aging kidney include decreased renal blood flow, due in part to atherosclerosis, resulting in a decreased GFR. Alterations in hormone levels including ADH, aldosterone, and ANP result in decreased urinary concentrating ability and alterations in the excretion of water, sodium, potassium, and acid. Under normal conditions, the aging kidney is able to maintain homeostasis. However, after abrupt changes in blood volume, acid load, or other insults, the kidney may not be able to function effectively because much of its renal reserve has been lost.

Kidney

¯Renal tissue

¯ # of nephrons and renal bld vessels; thickened basement mb of BC and Glomeruli

¯ Fnx of loop of Henle and Tubules

Assement findings:

Less palpable

¯Creatinine clearance

­ +BUN

­+Serum creatinine

Alterations in drug excretion

Nocuria

Loss of nrmal diurnal excretory patter due to ¯ability to concentrate urine

¯Urine vol

Ureter, Bladder, and Urethra

¯Elasticity and muscle tone

Weakening urinary sphincter

¯Bladder capacity and sensory receptors

Estrogen deviciency leading to thin, dry vaginal tissue

­+Prevalence of unstable

Prostataic enlargement

Assessment:

Palpable bladder after unrination due to retention

Streess incontinence (esp during Valsalva maneuver), dribbling urine after urination

Freq, urgency, nocturia, overflow incontinence

Stress of overactive bladder, dysuria (painful urination)

Overactive bladder

Hesitancy, freq, urgency, nocturia, straining to urinate, retention, dribbling

Assessment:

Palpable bladder after unrination due to retention

Streess incontinence (esp during Valsalva maneuver), dribbling urine after urination

Freq, urgency, nocturia, overflow incontinence

Stress of overactive bladder, dysuria (painful urination)

Overactive bladder

Hesitancy, freq, urgency, nocturia, straining to urinate, retention, dribbling

RENIN

Primary fnx: To increase BP and restore kidneys pressure perfusion

Secreted from juxtaglomerular cells

Released in response to decreased BV, BP or low renal Na+ (ATTEMPTS to increase BP)

Renin release causes production of Angiotensin II (a potent vaso-constrictor)

The renin-angiotensin-aldosterone system is a series of reactions designed to help regulate blood pressure.

1.When blood pressure falls (for systolic, to 100 mm Hg or lower), the kidneys release the enzyme renin into the bloodstream.

Renin is important in the regulation of blood pressure. Renin is produced and secreted by juxtaglomerular cells of the kidney (Fig. 45-4). 

The plasma protein angiotensinogen (from the liver) is activated to angiotensin I by renin. Angiotensin I is subsequently converted to angiotensin II by angiotensin-converting enzyme (ACE). ACE is located on the luminal surface of all blood vessels, with particularly high levels in the vessels of the lungs. Angiotensin II stimulates the release of aldosterone from the adrenal cortex, which causes Na+ and water retention, leading to an increased ECF volume. Angiotensin II also causes increased peripheral vasoconstriction. Release of renin is inhibited by an elevation in blood pressure brought about by increased ECF,vasoconstriction, and an increase in plasma sodium. Excessive renin production caused by impaired renal perfusion may be a contributing factor in the etiology of hypertension

Renin is released into the bloodstream in response to" decreased renal perfusion

decreased arterial blood pressure

decreased ECF

decreased serum Na+ concentration

increased urinary Na+ concentration.

What are the medications affecting BP regulation? What are the effects on kidney regulation?

• Thiazides and Thiazide-like diuretics
• Loop (high-ceiling diuretics)
• Osmotic diuretics
• Potassium-sparing diuretics
• Beta-blockers (a.k.a. Beta-adrenergic Blockers) “the –olols”
• ACE Inhibitors “the –prils”
• Calcium Channel Blockers

Thiazides and Thiazide-like diuretics

Thiazides and Thiazide-like diuretics- (HCTZ) Acts on the distal convoluted renal tubule, beyond the loop of Henle, to promote sodium, chloride, potassium, magnesium and water excretion. Used to tx HTN and peripheral edema. Used for clients with normal renal function.

Monitor for:

Hypercalcemia (b/c. Ca is reabsorbed),

Glucose tolerance.

Usually combined with other anti-HTN meds. MUST HAVE GOOD KIDNEY FNX

KNOW METABOLIC PANEL – ELECTROLYTES LEVEL BEFORE GIVING. Will have to replace if low.

1.     Decrease hypertension (lower blood pressure) and to

2.     Decrease edema (peripheral and pulmonary) in heart failure (CHF) and renal or liver disorders

Loop (high-ceiling diuretics)- acts on the ascending loop of Henle by inhibiting chloride transport of sodium into the circulation. Sodium and water are lost, together with potassium, calcium, and magnesium. Have little effect on the blood sugar. Uric acid level increases. More potent that thiazides as diuretics. Increases renal blood flow up to 40% (Lasix, Furosemide, Bumex, Torsemide) 

MBP – Metabolic panel.  Only wan to get rid of excess fluid. CREATINE CLEARANCE

Osmotic diuretics (Mannitol, Urea)-increases the osmolality (concentration) of the plasma and fluid in the renal tubules. Na, Cl, K, and water are excreted. Used to prevent renal failure, decrease ICP, IOP. INTRACRANIAL PRESSURE OR INTRAOCULAR PRESSURE

Potassium-sparing diuretics-

Potassium-sparing diuretics- weaker than thiazides and loop diuretic. Monitor for Hyperkalemia. (Aldactone, Aldosterone, Amiloride, Triamterene. Usually used with a diuretic.Never used with ACE inhibitors 

KEEPS POTASSIUM- RISK FOR HYPERKALEMIA

Beta-blockers (a.k.a. Beta-adrenergic Blockers)-reduces renin (enzyme) release. (Acebutolol, Atenolol, Betaxolol,

Metoprolol, all the suffix –olol)

CAN MASK S/S of  HYPOGLYCEMIa

ACE Inhibitors

ACE Inhibitors- tx HTN and CHF, blocks Angiotensin II and inhibits formation of Aldosterone (Benazepril, Captopril, Lisinopril, etc.) PRILS

HTN and CHF

c

Calcium Channel Blockers- decreases Calcium levels to promote vasodilation

Serum pH

↑↓

↑Alkalosis

↓Acidosis

135-145 mEq/L

↑Impaired Renal fnx

↓Diabetic ketoacidosis, diuretic therapy, water intoxication

Main extracellular electrolyte determining blood volume. Usually values stay within normal range until late stages of renal failure.

3.5-5.0

↑Renal failure, Addison's disease, diabetic ketosis, massive tissue destruction

↓Cushing syndrome, diarrhea
(severe), diuretic therapy,
gastrointestinal fi stula,
pyloric obstruction,
starvation, vomiting

Kidneys are responsible for excreting majority of body's potassium. In renal disease, K+ determinations are critical because K+ is one of the first electrolytes to become abnormal. Elevated K+ levels of >6 mEq/L can lead to muscle weakness and cardiac dysrhythmias.

6-20 mg/dl

↑Renal disease, increase in protein catabolism
(fever, stress),
urinary tract infection

↓Malnutrition, severe liver
damage

Blood urea nitrogen or BUN test is primarily used, along with the creatinine test, to evaluate kidney function in a wide range of circumstances, to help diagnose kidney disease, and to monitor patients with acute or chronic kidney dysfunction or failure. It also may be used to evaluate a person’s general health status when ordered as part of a basic metabolic panel

Creatinine Clearance

Creatinine urine

Creatinine serum

Serum Creatinine 0.2-1.0

Creatinine urine 6.0-2.0g/day

Creatinine clearance 59-137 ml/min/1.73m2

urin creatinine mg/ml x urine vol ml/min ÷Serum Creatinine mg/ml

Creatinine is a waste product of protein breakdown (primarily body muscle mass). Clearance of creatinine by kidney approximates the GFR.

Na

↑↓

135-145 mEq/L

Main extracellular electrolyte determining blood volume. Usually values stay within normal range until late stages of renal failure.

↑impaired renal fnx

↓Diabetic ketoacidosis, diuretic therapy water intoxication

1.5-2.5 mEq/L

↑Addison’s disease, hypothyroidism, absence of reflexes, resp failure and renal failure

↓Chronic alcoholism, severe
malabsorption

Magnesium is primarily excreted by the kidneys. Hypermagnesemia is generally not a problem unless the patient is ingesting magnesium (e.g., milk of magnesia, magnesium citrate, antacids containing magnesium). Clinical manifestations of hypermagnesemia can include absence of reflexes, decreased mental status, cardiac dysrhythmias, hypotension, and respiratory failure, People with kidney disease may not be able to excrete excess amounts of magnesium

22-26 mEq/L

Most patients in renal failure have metabolic acidosis and low serum HCO3– levels.

­ ↑Resp Acidosis, metabolic alkalosis

↓Resp alkalosis, metabolic acidosis

The anemia is due to decreased production of the hormone erythropoietin by the kidneys. Erythropoietin normally stimulates precursor cells in the bone marrow to produce RBCs (erythropoiesis). Other factors contributing to anemia are nutritional deficiencies, decreased RBC life span, increased hemolysis of RBCs, frequent blood samplings, and bleeding from the GI tract. Blood loss due to dialysis can be a contributing factor too

Homeostasis

Fluid regulation

Acid-base balance

Blood pressure control

Renin production (enzyme)

Erythropoietin production

Vitamin D activation

Filtration and excretion

Kidney Acid Base Balance

Secrete hydrogen ions

Reabsorb sodium and bicarbonate ions

Acidify phosphate salts

Produce ammonia

Acidosis pH < 7.35 (metabolic acidosis)

Alkalosis pH > 7.45 (metabolic alkalosis)

K. Na, P

 Sodium and salt should not be equated because the sodium content in 1 g of sodium chloride is equivalent to 400 mg of sodium.

Potassium restriction depends on the ability of the kidneys to excrete potassium. Most salt substitutes should be avoided if patients have been instructed to restrict potassium because they contain potassium chloride.

As kidney function deteriorates, phosphate elimination by the kidneys is diminished and the patient begins to develop hyperphosphatemia. Limit 1g/day

Monitor respiratory pattern for symptoms of respiratory difficulty (e.g., dyspnea, tachypnea, and shortness of breath) that are indicators of fluid excess.

Weigh patient daily and monitor trends to evaluate interventions.

Monitor intake and output to determine effect of treatment on kidney function.

Provide appropriate diet to help control edema and hypertension.

Instruct patient and/or caregivers on measures instituted to treat the hypervolemia (e.g., daily weights, fluid restrictions) to help monitor and control fluid overload and related hypertension

Color

      Dark hematuria

      Colorless  Excessive fluid, renal disease, or diabetes insipidus

Protein

      Persistent proteinuria – acute and cronic renal disease, esp involving glomeruli; heart failure

Glucose

      Glycosuria (excretion of glu in urine) – DM, low renal threshold for glu reabsorp

Ketones

      Prestent – Altered carb and fat metab in DM; dehydration

Specific gravity 1.003-1.030

            Low Dilute urine, excessive diuresis; diabetes insipidus

            High -  dehydration, glycosuria

Osmolality 300-1300 mOsm/kg

<300 Tubular dysfunction; kidney lost ability to concentrate or dilute urine (not part of routine urinalysis)

pH (urine) 4.0-8.0 (avg 6.0)  

            <4 Resp or metabolic acidosis

RBC 0.4/hpf

      >4 glomerulonephritis, kidney biopsy

WBC 0-5/hpf

      >5 UTI or inflammation

Urinalysis - General examination of urine to establish baseline information or provide data to establish a tentative diagnosis and determine whether further studies are to be ordered

Try to obtain first urinated morning specimen. Ensure specimen is examined within 1 hr of urinating. Wash perineal area if soiled with menses or fecal material.

59-137 ml/min/1.73m2

Creatinine is a waste product of protein breakdown (primarily body muscle mass). Clearance of creatinine by kidney approximates the GFR

Collect 24-hr urine specimen. Discard first urination when test is started. Save urine from all subsequent urinations for 24 hr. Instruct patient to urinate at end of 24 hr and add specimen to collection. Ensure that serum creatinine is determined during 24-hr period.

Reference interval: ≤50 mL urine (increases with age)

Residual - Determines amount of urine left in bladder after urinating. Finding may be abnormal in problems with bladder innervation, sphincter impairment, BPH, or urethral strictures.

If residual urine test is ordered, catheterize patient immediately after urinating or use bladder ultrasound equipment. If a large amount of residual urine is obtained, health care provider may want catheter left in bladder.

Urea nitrogen (BUN)

Used to identify presence of renal problems. Concentration of urea in blood is regulated by rate at which kidney excretes urea.

Reference interval: 6-20 mg/dL (2.1-7.1 mmol/L).

Be aware that when interpreting BUN, nonrenal factors may cause increase (e.g., rapid cell destruction from infections, fever, GI bleeding, trauma, athletic activity and excessive muscle breakdown, corticosteroid therapy).

Creatinine

More reliable than BUN as a determinant of renal function. Creatinine is end product of muscle and protein metabolism and is liberated at a constant rate.

Reference interval: 0.6-1.3 mg/dL (53-115 µmol/L).

Explain test and watch for postpuncture bleeding.

BUN/creatinine ratio

Reference interval: 12:1 to 20:1.

Uric Acid see Uric acid card

Fatigue
Headaches
Blurred vision
Elevated blood pressure
Anorexia
Nausea and vomiting
Chills
Itching
Excessive thirst
Change in body weight
Cognitive changes

Edema

acial (periorbital)
Ankle
Ascites
Anasarca
Sacral
Dysuria

Pain
Flank or costovertebral angle
Groin
Suprapubic

Female: 2.3-6.6 mg/dL (137-393 µmol/L)

Male: 4.4-7.6 mg/dL (262-452 µmol/L)

Higher than normal uric acid levels in the blood is called hyperuricemia and can be caused by the over-production of uric acid in the body or the inability of the kidneys to clear out enough uric acid

Used as screening test primarily for disorders of purine metabolism but can also indicate kidney disease. Values depend on renal function, rate of purine metabolism, and dietary intake of food rich in purines

Explain test and watch for postpuncture bleeding.

VITAMIN D

Activated in liver and kidneys

Activated Vitamin D is essential for absorption of calcium in GI tract

Renal failure can lead to alteration in Calcium and Phosphate balance

Radiology procedures
KUB, IVP, Retrograde pyelogram, renal angiogram, renal ultrasound, CT scan, etc.
Renal biopsy

Cystoscopy

KUB- to detect kidney stones
IVP- use contrast dye (nephrotoxic); check lesions obstructions
Renal US- check for masses
Bladder scan- check for residual urine
CT scan- use IV contrast.
Renal angiography- check renal vessels; use contrast
Renal biopsy- complication: hemorrhage

Prerenal

Intrarenal

Postrenal

Prerenal - heart/aorta

Intrarenal- Kidneys

Postrenal - Ureters/bladder

What are infections of the UT?

Upper and lower?

Lower UTI - cystitis (bladder inflammation) and erethritis (urethra)

Upper UTI - pylonephritis (kidney infection)

Most common UTI pathogen?

Counts indicating signifant UTI?

Minimal indicative count?

Patients at risk
Are immunosuppressed
Have diabetes
Have undergone multiple antibiotic courses
Have traveled to certain Third World countries

Hospital aquired UTI account for what %?

Cause of HA UTI?

Hospital-acquired UTI accounts for 31% of all nosocomial infections.
Causes
Often: E. coli
Seldom: Pseudomonas
Catheter-acquired UTIs
Bacterial biofilms develop on inner surface of catheter.

Urine for culture and sensitivity (if indicated)

Clean-catch sample preferred
Specimen by catheterization or suprapubic needle aspiration more accurate
Determine susceptibility of bacteria to antibiotics

Imaging studies
IVP or abdominal CT when obstruction suspected
Renal ultrasound for recurrent UTIs

Antibiotics
Selected on empiric therapy or results of sensitivity testing
Uncomplicated cystitis
Short-term course (1 to 3 days)
Complicated UTIs
Require long-term treatment (7 to 14 days)

Nitrofurantoin (Macrodantin)
Given 3 or 4 times a day
Long-term use
Pulmonary fibrosis
Neuropathies
Fluoroquinolones
Treat complicated UTIs
Example: Ciprofloxacin (Cipro)
Trimethoprim/sulfamethoxazole (TMP/SMX)
Used to treat uncomplicated or initial
Inexpensive
Taken twice a day
E. coli resistance to TMP-SMX ↑

What are two urinary analgesics?

What effect do they have?

Pyridium
Used in combination with antibiotics
Provides soothing effect on urinary tract mucosa
Stains urine reddish orange
Can be mistaken for blood and may stain underclothing
OTC

Urised
Used in combination with antibiotics
Used to relieve UTI symptoms
Preparations with methylene blue tint urine blue or green.

Inflammation of the bladder
ASSESSMENT FINDINGS:
Dysuria
Urinary frequency
Urinary urgency
Hematuria
Fever and chills
Increasing flank pain
Elevated WBC

Antibiotics Septra, Pyridium
Antipyretics
Antispasmodic
Force fluids
Proper hygiene
Bedrest
Treat underlying cause
Hospitalization- if acute

Infection/Inflammation of the urethra
ASSESSMENT FINDINGS:
Manifestations: same as cystitis, urethra tender, discharge present

Often associated with STD’s in men (gonorrhea), in women (chlamydia, trichomonas, monolilial).

Monitor VS, I/O
Increase fluid intake
 Collect sample
Antibiotics: Bactrim, Flagyl (trichomonas), Diflucan (monilial)

What are urinary Tract Calcul?

Risk factors?

Kidney stones

Metabolic
Abnormalities that result in increased urine levels of calcium, oxaluric acid, uric acid, or citric acid
Climate
Warm climates that cause increased fluid loss, low urine volume, and increased solute concentration in urine
Diet
Large intake of dietary proteins that increases uric acid excretion
Excessive amounts of tea or fruit juices that elevate urinary oxalate level
Large intake of calcium and oxalate
Low fluid intake that increases urinary concentration
Genetic Factors
Family history of stone formation, cystinuria, gout, or renal acidosis
Lifestyle
Sedentary occupation, immobility

The overall goals are that the patient with urinary tract calculi will have

(1) relief of pain

(2) no urinary tract obstruction

(3) knowledge of ways to prevent further recurrence of stones. (lo purines, oxalate, calcium.)

What is pyelonephritis?

Pathophysiology?

Pyelonephritis is an inflammation of the renal parenchyma (in renal medulla) and collecting system (including the renal pelvis). The most common cause is bacterial infection, but fungi, protozoa, or viruses sometimes infect the kidneys. Usually begins with colonization and infection of the lower urinary tract via the ascending urethral route

Infection spread by ascending microorganisms along the ureters or by way of bloodstream

Fever

chills

flank or low back pain
nausea, and vomiting

headache

malaise

painful urination

CVA tenderness

Diagnostic tests: CBC, WBC, STD’s testing, CT scan to detect abscess, US, KUB to check for tumor or cysts, IVP, UA/CS
Antibiotics
Anti-pyretics
Increase water intake
Treat underlying cause
Relieve obstruction if present

What is urinary incontinence?

Interventions?

uncontrolled leakage of urine. Among young adult to middle-aged women, the prevalence is 30% to 40% and it increases to 30% to 50% in older women

NOT a natural cause of aging

Interventions

Pelvic floor exercises and biofeedback with lifestyle modifications can help prevent or reverse incontinence

SIS R UFO

Stress Sudden increase in intraabdominal pressure causes involuntary passage of urine. (giving birth, lo estrogen, prostate surgery)

Incontinence after surgery and trauma - Vesicovaginal or urethrovaginal fistula may occur in women. (Fistulas)

Reflex -  occurs when no warning or stress precedes periodic involuntary urination. Spinal cord lesion above S2

Urge -involuntary urination is preceded by urinary urgency. Overactivity of detrusor muscle - CNS diseases

Functional - Loss of urine resulting from cognitive, functional, or environmental factors (elderly due to problems w/mobility and balance)

Overflow - when the pressure of urine in overfull

bladder overcomes sphincter control, obstruction or detrouser caused by myogenic or neurogenic factors (DM)

What is IVP?

Pre and post procedure care

Visualizes urinary tract after IV injection of contrast media.

Presence, position, size, and shape of kidneys, ureters, and bladder can be evaluated.

Cysts, tumors, lesions, and obstructions cause a distortion in normal appearance of these structures. Patient with significantly decreased renal function should not have IVP, because contrast media can be nephrotoxic and worsen renal function.*

Post care

Evening before procedure, give cathartic or enema to empty colon of feces and gas.

Assess for iodine sensitivity

Inform patient that procedure involves lying on table and having serial x-rays taken.

Advise patient that warmth, a flushed face, and a salty taste during injection of contrast material may occur.

Post procedure

Force fluids (if permitted) to flush out contrast media.

What is a renal biopsy?

pre and post procedure

Obtains renal tissue for examination to determine type of renal disease or to follow progress of renal disease. Technique is usually done as a skin (percutaneous) biopsy through needle insertion into lower lobe of kidney. Can be performed with CT or ultrasound guidance. Absolute contraindications are bleeding disorders, single kidney, and uncontrolled hypertension. Relative contraindications include suspected renal

infection, hydronephrosis, and possible vascular lesions.

Type and crossmatch patient for blood. Ensure consent form is signed.

Pre pocedure

Type and crossmatch patient for blood. Ensure Consent form

Ascertain coagulation status through patient history, medication history, CBC, hematocrit, prothrombin time, and bleeding and clotting time.

Discontinue anticoagulants

After procedure: Apply pressure dressing and keep on affected side for 30-60 min; bed rest for 24 hr.

Vital signs every 5-10 min,first hour.

Assess for flank pain, hypotension, decreasing hematocrit, ↑ temperature, chills, urinary frequency, dysuria, and serial urine specimens (gross/microscopic hematuria).

Urine dipstick can be used to test for bleeding in urine. Inspect biopsy site for bleeding. Instruct patient to avoid lifting heavy objects for 5-7 days and to not take anticoagulant drugs until allowed by health care provider.

What is a renal scan?

Pre and post procedure

valuates anatomic structures, perfusion, and function of kidneys. Radioactive isotopes are injected IV. Radiation detector probes are placed over kidney, and scintillation counter monitors radioactive material in kidney. Radioisotope distribution in kidney is scanned and mapped. Shows location, size, and shape of kidney and, in general, assesses blood flow, glomerular filtration, tubular function, and urinary excretion. Abscesses, cysts, and tumors may appear as cold spots because of presence of nonfunctioning tissue. Also used to monitor function of a transplanted kidney.

Requires no dietary or activity restriction. Inform patient that no pain or discomfort should be felt during test.

What is a KUB?

pre and post procedure

Involves x-ray examination of abdomen and pelvis and delineates size, shape, and position of kidneys. Radiopaque stones and foreign bodies can be seen.

Perform bowel preparation (if ordered).

What is an antegrade pyelogram (nephrostogram)

pre and post procedure

What is a renal arteriogram?

pre andpost procedure?

Visualizes renal blood vessels. Can assist in diagnosing renal artery stenosis additional or missing renal blood vessels, and renovascular hypertension. Can assist in differentiating between a renal cyst and a renal tumor. Also included in workup of a potential renal transplant donor. A catheter is inserted into the femoral artery and passed up the aorta to the level of the renal arteries (Fig. 45-9). Contrast media is injected to outline the renal blood supply.*

Before procedure: Prepare patient the prior evening by giving cathartic or enema. Before injection of contrast material, test for iodine sensitivity. The patient may experience a transient warm feeling along the course of the blood vessel when contrast media is injected. After procedure: Place a pressure dressing over femoral artery injection site. Observe site for bleeding. Have patient maintain bed rest with affected leg straight. Take peripheral pulses in the involved leg every 30-60 min to detect occlusion of blood flow caused by a thrombus. Observe for complications including thrombus, embolus, local inflammation, and hematoma.

Med for chronic renal failure

Epogen

Procrit

Man-made epoetin alfa called colony-stimulating factor to stimulate cells in the bone marrow to multiply and produce RBC

 Target patient with HGB 10-12

The erythropoietin that is used for therapy, called epoetin alfa, is man-made. It is a product of the genetic engineering of ovarian cells of the Chinese hamster and is produced through recombinant DNA technology in bacteria. It does not cure the underlying cause of the anemia, and unless the underlying cause can be reversed, treatment with epoetin alfa must be continued indefinitely. Epoetin alfa belongs to a class of drugs called colony-stimulating factors because of their ability to stimulate cells in the bone marrow to multiply and form colonies of identical cells

Natriuretic Hormone: The right atrium of the heart releases this in response to increased volume and stretch (preload bld load in ventricle at end of diastole)

Inhibits ADH secretion so that the collecting tubules in the kidney are less porous and a larger amount of urine is thus produced (decreasing preload)

Increase aldosterone= decrease in urine output

Post- surgery: Increased ADH release=increase in water reabsorption= decrease in urine output

Anesthesia and/or narcotics= decrease bladder fullness sensation

More water reabsorbed less excreated

Cytoscopy?

Pre and postcare?

Inspects interior of bladder with a tubular lighted scope (cystoscope) Can be used to insert ureteral catheters, remove calculi, obtain biopsy specimens of bladder lesions, and treat bleeding lesions. Lithotomy position is used. Procedure may be done using local or general anesthesia, depending on needs and condition of patient. Complications include urinary retention, urinary tract hemorrhage, bladder infection, and perforation of the bladder

Before procedure: Force fluids or give IV fluids if general anesthesia is to be used. Ensure consent form is signed. Explain procedure to patient. Give preoperative medication.

Prepocedure

Force fluids or give IV fluids if general anesthesia is to be used. Ensure consent form is signed. Explain procedure to patient. Give preoperative medication.

Postprocedure

Explain that burning on urination, pink-tinged urine, and urinary frequency are expected effects. Observe for bright red bleeding which is not normal. Do not let patient walk alone immediately after procedure because orthostatic hypotension may occur. Offer warm sitz baths, heat, mild analgesics to relieve discomfort.

Renal CT?

Pre and postprocedure?

Visualization of kidneys.

Size

Tumors

Abscesses

Suprarenal masses (e.g., adrenal tumors, pheochromocytomas)

Obstructions

Advantage of CT over ultrasound is its ability to distinguish subtle differences in density.

Use of IV-administered contrast media during CT accentuates density of renal tissue and helps differentiate masses

Preprocedure 

Iodine sensitivity.

Lie very still during the procedure while the machine takes precise transaxial images.

Sedation may be required if patient is unable to cooperate.

No postprocedure