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URINARY SYSTEM: QUICK REVIEW URETERS, BLADDER,URETHRA

REVIEW OF URINARY ANATOMY &


PHYSIOLOGY
• Located:
– Under back muscles
– Behind peritoneum
• Thus: retroperitoneal
– Below level 2of lowest ribs
– Right lower than left
– Adrenal gland on top of
kidney
• Medulla
– Contains Pyramids &
Papilla
• Pelvis  Bladder capacity 400 - 500 mL
– Calyx = division of pelvis  smooth muscle
• Pleural = calyces  Urethral sphincter
• Cortex  Micturition
 Efflux of urine

URINE FORMATION
 1- Glomerular filtration 2-Tubular reabsorption, 3-
Tubularsecretion
 Amino acids and glucose are usually filtered at the level
of the glomerulus and reabsorbed
 renal glycosuria
 Proteinuria (usually lowmolecular weight proteins)

 Each kidney has 1 million


 If total number of functioning nephronsis less than 20%
of normal renal replacement therapy needed
 Nephrons
 Cortical nephrons- 80% to 85%
GLOMERULAR FILTRATION
 normal blood flow through the kidney1000 and
 Juxtamedullary nephrons- 15% to
1,300mL/min
 20%
 99% of filtrate is Glomerular Filtration reabsorbed
 Glomerulus
 Bowman’s Capsule
ADH (Antidiuretic Hormone)
 Made in hypothalamus; water conservation hormone
 Stored in posterior pituitary gland
 Acts on renal collecting tubule to regulate reabsorption
or elimination of water
 If blood volume decreases, then ADH is released &
water is reabsorbed by kidney. Urine output will be
lower but concentration will be increased.
Volume of urine also controlled by glomerular filtration rate
RENIN  Unique arrangment of blood vessels
 Released by kidneys in response to decreased blood
volume – Afferent arteriole -----to----capillary bed-----to----efferent
 Causes angiotensinogen (plasma protein) to split & arteriole -----to-----capillary bed ----to---- veins
produce angiotensin I
 Lungs convert angiotensin I to angiotensinII  First capillary bed = glomerular capillaries
 Angiotensin II stimulates adrenal gland to release  Second capillary bed = peritubular capillaries
aldosterone & causes an increase in peripheral  Purpose of this = to control the pressure in the
vasoconstriction glomerular capillaries & consequently the glomerular
filtration pressure
3 factors control this:
(1) autoregulation
 Local feedback from muscle tension in afferent
arteriole
 Local feedback from DCT at JGA
 Mediated via endothelial secretions of glomerular
capillaries
(2) sympathetic nervous system
(3) Renin

Regulation of Red Blood Cell Production


 kidneys detect a decrease inthe oxygen tension-release
ERYTHROPOIETIN.
Vitamin D Synthesis
 kidneys are responsible forthe final conversion of • B = increase fluid volume; overhydration; high output heart
inactive vitamin D to its activeform, 1,25 failure
dihydroxycholecalciferol. • C = kidney pathology
Secretion of Prostaglandins • D = hypertension; arteriolar spasm
 kidneys produce prostaglandin E and prostacyclin, which
have a vasodilatory effect and are important in
maintaining renal blood flow.
Excretion of Waste Products
 kidneys eliminate the body’s metabolic waste products.
 The major waste product ofprotein metabolism: urea, of
(about 25 to 30 g)
 Other wastes: creatinine,phosphates, and sulfates,
uricacid, drug metabolites
Urine storage
 filling and emptying of the bladder are mediated by
coordinated sympathetic and parasympathetic nervous
system
 parasympathetic pelvic nerves at the level of S1 through
S4
 150 to 200 mL- sensation of fullness
 300 mL to 500 mL - strong desired to void
Bladder Emptying – Hormones help control the volume of urine via fluid &
 Initiation of voiding - efferent pelvic nerve, which electrolyte balance
originates in the S1 to S4 area • The concentration factor essentially deals with urine
 micturition- mediated by muscarinic an cholinergic volume
receptors within the detrusor – Usually more the volume = more the dilution [a direct
 pressure during micturition 20 40 cm H2O proportion]
1. Aldosterone • rapid decline leads to ESRD
 From adrenal cortex • Prognosis : excellent
 Works on distal convoluted tubule NURSING MANAGEMENT
 Causes H2O & Na+ retention • intake and output monitoring
2. Atrial natriuretic hormone(ANH) • patient education of the disease and
 From atrial wall of heart Treatment
 Works on distal convoluted tubule CHRONIC GLOMERULONEPHRITIS
 Works in opposition to aldosterone
 Causes H2O & Na+ loss • repeated occurrence of acute nephriticsyndrome,
3. Antidiuretic hormone nephrosclerosis, glomerular sclerosis
 From posterior pituitary CLINICAL MANIFESTATIONS
 Works on collecting tubules • poorly nourished
 Causes reabsorption of H2O (Na+ goes with it) • yellow-gray pigmentation of the skin
•Peripheral and periorbital edema
• BP maybe normal or elevated
RENAL DISORDERS • cardiomegaly may be present
• crackles and rale
NEPHROSCLEROSIS •Peripheral neuropathy and diminished DTR
ASSESSMENT AND DIAGNOSTIC FINDINGS
 hardening of renalarteries due toprolonged • urine sg 1.010
 hypertension or DM • presence of urinary casts
TWO FORMS •GFR of 50 ml/min
• Malignant • chest x-ray : cardiac enlargement
- occurs in young adults (2x in men than women) • MRI : decreased size of of renal cortex
- associated with hypertension MEDICAL MANAGEMENT
• Benign • diuretic medications
- occurs in older adults • Sodium and water restrictions
- Associated with atherosclerosis and hypertension • weight monitoring
ASSESSMENT FINDINGS • early dialysis
◦ Hematocrit NURSING MANAGEMENT
◦ Creatinine • relieve anxiety
◦ Serum potassium • provide emotional support
◦ Serum calcium • self-care needs
◦ Lipid panel •Follow-up evaluations
◦ Blood glucose NEPHROTIC SYNDROME
◦ Urinalysis
◦ Urinary albumin-to-creatinine ratio •A renal failure manifested by massiveproteinuria,
MEDICAL MANAGEMENT hypoalbuminemia, highserum cholesterol and hyperlipidemia
•ACE inhibitors • any condition that damages the capillarymembrane and
• treat underlying cause results in increasedglomerular permeability to plasma
protein
ACUTE NEPHRITIC SYNDROME CLINICAL MANIFESTATIONS
• glomerular inflammation • presence of edema (soft and pitting)
• causing passage of protein in urine (2 to 3 g per day) • irritability
• a combination of protein range proteinuria • headache
CLINICAL MANIFESTATIONS • malaise
• azotemia ASSESSMENT AND DIAGNOSTIC FINDINGS
• microscopic hematuria • proteinuria (3.5 g/day)
• edema • presence ofWBC in urine
• proteinuria • epithelial casts in urine
• cola-colored urine • renal biopsy
• Severe cases MEDICAL MANAGEMENT
•Headache • treat underlying conditions
• malaise • prevention of CKD
• flank pain • prescribing diuretics
• engorged neck veins •ACE inhibitors
• pulmonary edema and cardiomegaly • antilipidemic agents
ASSESSMENT AND DIAGNOSTIC FINDINGS
• enlargement of kidneys
• elevated IgA
• biopsy
COMPLICATIONS
• hypertensive encephalopathy
CLINICAL MANIFESTATIONS
• lethargic and appear critically ill
• dry mucous membranes
• headache, drowsiness
• muscle twitching and seizures
ASSESSMENT AND DIAGNOSTIC FINDINGS

POLYCYSTIC KIDNEY DISEASE

• presence of cysts in the kidney •Scanty to normal volume


• may be inherited • urine specific gravity is low
•Autosomal dominant /recessive PKD • Inability to concentrate urine is the earliest sign of kidney
CLINICAL MANIFESTATIONS damage
• increasing size of kidneys • anatomic changes in kidney in CT scan or MRI
•Hematuria •Progressive metabolic acidosis Prevention
• polyuria • provide adequate hydration
• hypertension • prevent and treat shock promptly
• renal calculi • treat hypotension promptly
• fullness and flank pain • assess renal function continuously
ACUTE RENAL FAILURE • treat infections promptly
• treat sepsis
• acute renal failure (ARF) •Prevent toxic drug effecs
• rapid loss of renal function due to damage MEDICAL MANAGEMENT
• potentially life-threatening • hemodialysis / peritoneal dialysis / CRRT
• increase in serum creatinine of 50% • may have oliguria, • treatment of hyperkalemia (usage of Kayexalate)
nonoliguria, or anuria • proper ventilation
ACUTE RENAL FAILURE • phosphate-binding agents
• CATEGORIES •Nutritional therapy
• Prerenal
• Intrarenal NURSING MANAGEMENT
• Postrenal • monitoring fluid and electrolyte imbalance
• reducing metabolic rate
• promoting pulmonary function
• preventing infection
• providing skin care
• provide psychosocial support
INFECTIONS OF THE URINARY TRACT

URINARY TRACT INFECTIONS


• caused by pathogenic microorganisms
• classified either lower UTI and upper UTI
• second most common infection in the body
• cases common in women (1 out of 5)
• urinary tract is the most common site for nosocomial
infections UTIs
•Lower UTI
• cystitis
• prostatitis
• bacterial urethritis
• Upper UTI
• pyelonephritis
• incontinence
• nocturia
• Suprapubic or pelvic pain
•Complicated UTI
• Sepsis or shock
ASSESSMENT AND DIAGNOSTIC FINDINGS
• Urine cultures
• Groups of patients to have urine culture when bacteriuria is
present
• all children all men DM patients
• recent instrumentation and hospitalized
• pregnant women postmenopausal women
• sexually active or with new sexual partners
•3 or more recent UTI in a year
ASSESSMENT AND DIAGNOSTIC FINDINGS
• pyuria (WBC 4 /hpf) • CT scan for abscesses
• ultrasound for obstruction
•Cystourethroscopy
MEDICAL MANAGEMENT

LOWER UTI: PATHOPHYSIOLOGY


• Bacterial invasion of the urinary tract
• Deactivation of glycosaminoglycan (GAG)
• absence of normal bacterial flora of the vagina and
urethra
• absence if immunoglobulin A (IgA)
• Reflux
• urethrovesical reflux
• ureterovesical reflux

NURSING MANAGEMENT
• relieving pain
• increase fluid intake
• remove urinary tract irritants
• encourage frequent voiding
• Monitoring potential complications
• bacteriuria • use strict aseptic technique when inserting catheters
• more than 105 colonies of bacteria per ml of • securing catheters
urine • maintaining a closed system
• Routes of infections • perineal care
• transurethral route • teaching self-care
• bloodstream UPPER UTI
• fistula • Pyelonephritis
CLINICAL MANIFESTATIONS • acutely ill with fever and chills
• 50% with bateriuria do not manifest symptoms • leukocystosis
• s/s of uncomplicated lower UTI • flank pain
• burning on urination • nausea and vomiting
• increased frequency
PYELONEPHRITIS: ASSESSMENT
•CT scan
• IV pyelogram
• radionuclide imaging
• urine culture and sensitivity testst
PYELONEPHRITIS: MEDICAL MANAGEMENT
• medications for UTI (table)
• hydration with oral or parenteral fluids
PYELONEPHRITIS: NURSING MANAGEMENT
• increase OFI
• VS q4
• medications as ordered
• emptying bladder frequently
• proper perineal hygiene
•Adherence to treatment regimen

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