ARF, CRF, ESRD, AGN, NEPHROTIC SYNDROME, URETHRAL STRICTURE, RENAL CALCULI

1. Mr. MaheshChand
Tutor

2. content
Reviewof anatomy and physiology of genitourinary system
Etiology, pathophysiology, clinical manifestations,diagnosis,
medical and surgical treatment modalities, alternative
therapies, dietetics and nursing management
Urological obstructions-
Urethral strictures
Renal calculi
Nephrosis

3. content
Disorders of kidney-
Nephrotic syndrome
Acute renal failure
Chronic renal failure
End stage renal disease
Dialysis, renal transplant
Cancer of kidney
Congenital disorder

4. content
Disorders of Ureters, urinary bladder andurethra-
UTI
Cystitis
Urinary incontinence
Urinary retention
Urinary bladdercalculi
Urethirtis
Urethral tumors
Ureteral calculi
Trauma of Ureters, bladder,urethra
Congenital disorders of ureters, bladder andurethra

5. anatomy and physiology of
genitourinary system

7. anatomy and physiology of
genitourinary system

8. physiology of genitourinary system

11. anatomy and physiology of
genitourinary system
Nursing assessment: history, and physicalexamination


12. urological obstructions
urethral strictures
A urethral stricture is a scar in or around
the urethra, which can block the flow of
urine, and is a result of inflammation,
injury or infection.

13. Anatomy of the Male Reproductive System
urological obstructions

14. urological obstructions
Risk factors-
Urethral strictures are more common in men because
their urethras are longer than those in women.
Thus men's urethras are more susceptible to disease
or injury.
 A person is rarely born with urethral strictures and
women rarely develop urethral strictures.

15. urological obstructions
Etiology -
Stricture disease may occur anywhere from the
bladder to the tip of the penis.
 The common causes of stricture are trauma to the
urethra and infections such as sexually transmitted
diseases and damage from instrumentation.
Trauma such as straddle injuries, direct trauma to
the penis and catheterization can result in strictures
of the anterior part of the urethra.

16. urological obstructions
Etiology -
In adults, urethral strictures from instrumentation
trauma may occur after prostate surgery and urinary
catheterization.
 In children, urethral strictures most often follow
reconstructive surgery for congenital abnormalities
of the penis and urethra, cystoscopy and
occasionally may be congenital.

17. urological obstructions
Clinical features -
painful urination.
slow urine stream.
decreased urine output.
spraying of the urine stream.
blood in the urine.
abdominal pain.
urethral discharge.
urinary tract infections in men..

18. urological obstructions
Diagnostic evaluation-
• History Collection
• Blood test
• Physicalexamination.
• Urethral imaging (X-rays orultrasound).
• Retrograde urethrogram

19. Normal Urethrogram Obstructive Urethrogram
urological obstructions

20. urological obstructions
Treatment-
• Enlarging the stricture by gradual stretching
(dilation).
• Urethrotomy: Cutting the stricture with a
endoscopic equipment
• Urethroplasty surgical repair of the stricture with
reconnection and reconstruction.
• Urethral Stents where a biocompatible hollow
tube is placed on the inside of the stricture to
allow for free passage of urine.

21. urological obstructions
renal calculi
Urolithiasis refers to stones (calculi) in the
urinary tract.
Stones are formed in the urinary tract when
concentrations of substances such as calcium
oxalate, calcium phosphate, and uric acid
increase.

22. urological obstructions
Types of stone-
Calcium stone
Uric acid stone
Cystiene stone
Struvite stone

23. urological obstructions
Types of stone-
Calcium stone:
• Most stones (75%) are composed mainly of calcium oxalate
crystals.
• Increased calcium concentrations in blood and urine promote
precipitation of calcium and formation of stones.
• Cellulose sodium phosphate (Calcibind) may be effective in
preventing calcium stones.
• Therapy with thiazide diuretics may be beneficial.

24. urological obstructions
Uric acidstones:
• 5% to 10% of all stones
• Gout
• Diet high in purines and abnormal purine metabolism.
• Low-purine diet such as shellfish, asparagus,
mushrooms, and organ meats are avoided.
• Allopurinol may be prescribed to reduce serum uric
acid levels and urinary uric acid excretion.
• Proteins may be limited in diet

25. urological obstructions
Struvite stones:
• 15% of urinary calculi
• Struvite stones are made of magnesium, ammonium and
phosphate
• Form in persistently alkaline, ammonia-rich urine
• Caused by the presence of urease splitting bacteria
such as Proteus, Pseudomonas, Klebsiella, Staphy-
lococcus, or Mycoplasma species.

26. urological obstructions
Cystine stones:
1% to 2% of all stones
Occur in patients with a rare inherited defect
in renal absorption of cystine (an amino acid).
Penicillamine is administered to reduce the
amount of cystine in the urine.
Low-protein diet

27. Urological obstrUctions
Causes and predisposing factors:
Chronic dehydration, poor fluid intake, andimmobility
Living in mountainous and desert areas
Infection, urinary stasis, and periods ofimmobility
Medications- antacids, acetazolamide (Diamox),
vitamin D, laxatives, and high doses of aspirin

28. Urological obstrUctions
Location of stones-
Kidney
Ureter
Bladder
Urethra

29. Urological obstrUctions
Site of obstruction-

30. Urological obstrUctions
Clinical features-
Pain that radiates to the lower abdomen and groin
Heamturia
Dysuria
Oedema
Pyuria
Nausea, vomiting, diarrhea, abdominal discomfort
Chills and fever (may)

31. Urological obstrUctions
renal calcUli
Diagnostic evaluation-
• History
• Physical examination
• Blood studies
• Urinalysis
• IVP
• Cystoscopy
• Radiographic studies

32. Urological obstrUctions
Management
General Principles
If small stone (< 4 mm) and able to treat as outpatient,
80% will pass stone spontaneously with hydration, pain
control, and reassurance.
Hospitalized for intractable pain, persistent vomiting,
high-grade fever, obstruction with infection, and solitary
kidney with obstruction.
Medical management
Surgical management
Nursing management

33. Urological obstrUctions
Medical management:
• Opioid analgesics or NSAIDs are administered.
• NSAIDs provide specific pain relief because they inhibit the
synthesis of prostaglandin E.
• Hot baths or moist heat to the flank areas may also be useful.
• Fluids are encouraged. This increases the hydrostatic
pressure behind the stone, assisting it in its downward
passage.
• A high, around-the-clock fluid intake reduces the
concentration of urinary crystalloids, dilutes the urine, and
ensures a high urine output.

34. Urological obstrUctions
renal calcUli
 N o n surgicalmanagement-
Ureteroscopy
ESWL (Extra Corporeal Shock wave lithotripsy)
Endoscopic procedures
Electrohydrolic lithotripsy
Chemolysis

35. Urological obstrUctions
Ureteroscopy
 Ureteroscopy involves visualizing the stone and then destroying it.
 Access to the stone is accomplished by inserting a ureteroscope into the
ureter and then inserting a laser, electrohydraulic lithotriptor, or
ultrasound device through the ureteroscope to fragment and remove the
stones.
 A stent may be inserted and left in place for 48 hours or more after the
procedure to keep the ureter patent

36. Urological obstrUctions
ESWL-
ESWL is a noninvasive procedure used to break up stones in
the calyx of the kidney
In ESWL, a high-energy amplitude of pressure, or shock wave,
is generated by the abrupt release of energy and transmitted
through water and soft tissues.
When the shock wave encounters a substance of different
intensity (a renal stone), a compression wave causes the
surface of the stone to fragment.
Repeated shock waves focused on the stone eventually reduce
it to many small pieces. These small pieces are excreted in the
urine, usually without difficulty.

37. Urological obstrUctions
ESWL-

38. Urological obstrUctions
Endoscopic procedures-
 A percutaneous nephrostomy or a percutaneous
nephrolithotomy may be performed, and a nephroscope is
introduced through the dilated percutaneous tract into the
renal parenchyma.
Depending on its size, the stone may be extracted with
forceps or by a stone retrieval basket. Alternatively, an
ultrasound probe may be introduced through the
nephrostomy tube.

39. Urological obstrUctions
Electrohydraulic lithotripsy-
an electrical discharge is used to create a
hydraulic shock wave to break up the stone.
 A probe is passed through the cystoscope, and
the tip of the lithotriptor is placed near
the stone
 This procedure is performed under
topical anesthesia.

40. Urological obstrUctions
Chemolysis-
Chemolysis, stone dissolution using infusions of
chemical solutions (eg, alkylating agents,
acidifying agents)
A percutaneous nephrostomy is performed, and
the warm irrigating solution is allowed to flow
continuously onto the stone.

41. Urological obstrUctions
Surgical management
 Nephrolithotomy - Incision into the kidney with
removal of the stone
 Nephrectomy –
 Pyelolithotomy -
Ureterolithotomy -
Cystostomy –
removal of kidney
removal of stone from renal pelvis
removal of stone from ureter
removal of stone from bladder
Cystolitholapaxy - an instrument is inserted through the
urethra into the bladder, and the stone is crushed in the
jaws of this instrument

42. DisorDers of kiDney
glomerUlonephritis
(acUte nephritic synDrome )
Definition –
Acute glomerulonephritis refers to a group of
kidney diseases in which there is an
inflammatory reaction in theglomeruli.

43. DisorDers of kiDney
Risk factors and Causes–
• Group A beta- hemolytic streptococcal infection in the
throat
• Impetigo (infection of the skin)
• Acute viral infections-URTI, mumps, varicella zoster virus,
Epstein-Barr virus, hepatitis B, and human immunodeficiency
virus [HIV] infection).
• Antigens outside the body (eg, medications, foreignserum)
• High blood pressure
• Diabetic kidney disease (diabetic nephropathy

44. DisorDers of kiDney

45. DisorDers of kiDney
Clinical features-
Hematuria - The urine may appear cola-colored be-
cause ofred blood cells (RBCs)
Edema andhypertension
Oliguria
Anemia from loss of RBCs into theurine

46. DisorDers of kiDney
Clinical features-
 I n the more severe form of the disease, patients
also complain of headache, malaise, and flank pain.
 Elderly patients may experience circulatory
overload with dyspnea, engorged neck veins,
cardiomegaly, and pulmonary edema.
Atypical symptoms include confusion, and
seizures, which are often confused with the
symptomsof a primary neurologicdisorder

47. DisorDers of kiDney
Diagnostic evaluation-
History
 O n examination- kidney is large, tender, edematous and
congested
Urinanalysis- protienuria, hematuria , oliguria
Blood studies-
Serum creatinine, BUN increased
Hypoalbuminemia, hyperlipidemia
 Antistreptolysin O titers are usually elevated in post
streptococcal glomerulonephritis
Electron microscopy analysis help identify the nature of the
lesion.
Kidney biopsy may be needed for definitive diagnosis.

48. DisorDers of kiDney
Complications-
Hypertensive Encephalopathy
Heart Failure
Pulmonary Edema
ESRD

49. DisorDers of kiDney
Management-
Goal-
To conserve renal function
To treat complication adequately
Types of management-
Non pharmacological management
Dietary management
Pharmacological management
Nursing management

50. DisorDers of kiDney
Non pharmacological management-
Complete bed rest – as excessive activity may increase
the proteinuria and hematuria. It should be encouraged
until the urine clears and BUN, creatinine and BP
return to normal.
Strict intake out put charting.
Fluid restrictions
Plasmapheresis to decrease the serum anti body level.
Dialysis if, uremic symptoms are severe.

51. DisorDers of kiDney
Dietary management-
Protein restricted diet as the level of BUN and
creatinine is high in blood
 L o w fat diet due tohyperlipidemia
Sodium restriction if hypertension, edema or
congestive heart failure are present.
 Increased carbohydrate diet to provide energy
and to prevent the catabolism of protein.

52. DisorDers of kiDney
Pharmacological management-
Residual streptococcal infection is suspected,
penicillin is the agent of choice.
Diuretics and antihypertensive agents may be
given to control hypertension.
Corticosteroids and cytotoxic agents are used to
reduce the inflammation.
 H 2 blockers (to prevent stress ulcers)
 Phosphate binding agents (to reduce phosphate
and elevate calcium).

53. DisorDers of kiDney
Nursing management-
Monitor vital signs, intake and output, and maintain
dietary restrictions during acute phase.
Encourage rest during the acute phase as directed until
the urine clears and BUN, creatinine, and blood pressure
normalize.
Administer medications as ordered, and evaluate
patient's response to antihypertensives, diuretics, H2
blockers, phosphate-binding agents, and antibiotics (if
indicated).

54. DisorDers of kiDney
Nursing management-
Regular monitoring of blood pressure, urinary
protein, and BUN concentrations
Encourage patient to treat any infection
promptly.
Tell patient to report any signs of decreasing
renal function and to obtain treatment
immediately.

55. DisorDers of kiDney
nephrotic synDrome
Definition-
Nephrotic syndrome is a clinical disorder characterized by
marked increase of protein in the urine (proteinuria),
decrease in albumin in the blood (hypoalbuminemia),
edema, and excess lipids in the blood (hyperlipidemia).
These occur because of increased permeability of the
glomerular capillary membrane.

56. Etiology:
Minimal change disease
Diabetic kidney disease
Systemic lupus erythematous
Heart failure ( right side HF)
Medications
Certain infections ( hepatitis B and C, HIV,malaria)

58. Clinical features-

59. Diagnostic evaluation-
Urinalysis- marked proteinuria, microscopic hematuria,
24-hour urine for protein (increased)
Protein electrophoresis and immunoelectrophoresis of
the urine to categorize the proteinuria
Needle biopsy of kidney for histologic examination of
renal tissue to confirm diagnosis.
Serum chemistry- decreased total protein and albumin,
normal or increased creatinine, increased triglycerides,
and altered lipid profile

60. DisorDers of kiDney
nephrotic synDrome
Management-
Treatment of causative glomerulardisease
Diuretics and angiotensinconverting enzyme
inhibitors to control proteinuria
Corticosteroids or immunosuppressant agents todecrease
proteinuria
General management ofedema
Sodium and fluid restriction; liberalpotassium
Dietary proteinsupplements

61. DisorDers of kiDney
nephrotic synDrome
Nursing Management-
Monitordaily weight, intake and output, and urine specific
gravity.
Monitor CVP (if indicated), vital signs, orthostaticblood
pressure, and heart rate to detecthypovolemia.
Monitor serum BUN and creatinine toassess renal function.
Administer diuretics or immunosuppressants asprescribed,
and evaluate patient's response.
Infuse I.V. albumin asordered.
Encourage bed rest for a few days to help mobilizeedema;
however, some ambulation is necessary to reduce risk of
thromboembolic complications.

62. DisorDers of kiDney
acute renal failure
Definition-
Acute renal failure is a sudden and almost complete
loss of kidney function caused by failure of renal
circulation or by glomerular or tubular dysfunction.

63. DisorDers of kiDney
acute renal failure
Etiology-
 P r e – renal (hypoperfusion of kidney)
Intra – renal (actual damage to the kidneytissue)
Post – renal (obstruction to urineflow)

64. DisorDers of kiDney
acute renal failure
Etiology-
 P r e –renal
Hemorrhage
Renal loses
GI losses
Impaired cardiac efficiency
sepsis
Anaphylaxis
Antihypertensive medications

65. DisorDers of kiDney
acute renal failure
Etiology-
Intra –renal
Prolonged renal ischemia
Nephrotoxic agents
Aminoglycosides agents
Radiopaque contrast agents
Heavy metals
Solvents and chemicals

66. DisorDers of kiDney
acute renal failure
Etiology-
Post –renal
Urinary tract obstructions
Renal calculi
Tumors
BPH
Blood clots
Strictutres

67. DisorDers of kiDney
acute renal failure
PHASES OFARF
Initiating phase
Oliguric phase
Diuretic phase
Recovery phase

68. DisorDers of kiDney
acute renal failure
PHASES OFARF
Initiating phase
Begins with the initial insult and ends when oliguria develops
Oliguric phase
Urine output less than 400 ml/day
Diuretic phase
Urine out put become normal but nitrogenous waste products
still remain elevated in blood
Recovery phase
It signifies the improvement of renal function
It takes 3-12 months to return normal

69. DisorDers of kiDney
acute renal failure
Clinical features-
Vomiting and/or diarrhea, which may lead to dehydration.
Nausea.
Weight loss.
pale urine.
Less frequent urination, or in smaller amounts thanusual,
with dark coloured urine
Haematuria.
Pressure, or difficulty urinating.
Itching.

70. DisorDers of kiDney
acute renal failure
Clinical features-
Bone damage.
Muscle cramps (caused by low levels of calcium whichcan
cause hypocalcaemia)
Muscle paralysis.
Swelling of the legs, ankles, feet, face and/or hands.
Shortness of breath due to extra fluid on the lungs
Pain in the back orside
Feeling tired and/or weak.

71. DisorDers of kiDney
acute renal failure
Clinical features-
Memory problems.
Difficulty concentrating.
Dizziness.
 L o w bloodpressure.
Anorexia
Seizures (if blood urea nitrogen level is very high)

72. DisorDers of kiDney
acute renal failure
Diagnostic evaluation-
History regarding the etiological factors and risk factors.
Physical symptoms
Urine output – scanty, bloody, and low specific gravity
Increased BUN and creatinine level in blood
Hyperkalemia
Metabolic acidosis
Hyperphoshatemia
Hypocalcemia
Anemia

73. DisorDers of kiDney
acute renal failure
Management-
• Antihypertensive agents
• Diuretics
• Sodium polystyrene sulfonate (Kayexalate)
• Fluid and electrolyte replacement
• Dialysis
• To correct dehydration.
• To Keep other body systems working properly

74. Chronic renal Failure
CRF or ESRD is a progressive, irreversible deterioration in
renal function in which the body’s ability to maintain
metabolic and fluid and electrolyte balance fails resulting in
uremia or azotemia.

75. Etiology
• Diabetes mellitus
• Hypertension
• SLE
• Sickle cell disease
• Glomerulonephritis
• Pyelonephritis
• ARF
• Infections

76. PATHPHYSIOLOGY
DUE TO ETIOLOGICAL FACTORS
DECREASED GFR
HYPERTROPHY OF REMAINING NEPHRONS
INABILITY TO CONCENTRATE URINE
FURTHER LOSS OF NEPHRON FUNCTION
LOSS OF NON-EXCRETORY AND EXCRETORY
FUNCTION

77. STAGES OF CRF
1) Reduced Renal reserve
- BUN is high or normal
- Client has no C/M
- 40 to 75 % loss of nephron function
2) Renal Insufficiency
-75 to 90 % loss of nephron function
-Impaired urine concentration
-Nocturia, mild anemia, increased
creatinine and BUN

78. 3) Renal failure
- Severe azotemia
- Impaired urine dilution
- Severe anemia
-Electrolyte Imbalances
Hypernatremia
Hyperkalemia
Hyperphosphatemia
4) End Stage Renal Disease
-10 percentage nephrons functioning
-Multisystem dysfunction

79. Clinical Manifestations of CRF
Electrolyte and acid-base balance
-Anemia
-Bleeding Tendencies
-Infection
-Weight loss
-Nausea and vomitting

80. DIAGNOSTIC STUDIES
 History and physical examination
 Routine lab measurements
- BUN
- Serum Creatinine
- Serum Electrolytes
- Hematocrit and Hb levels
- Urine Analysis
- Urine Culture
Radiological:
- Renal Ultrasound
- Renal Scan
- C T Scan
- Renal Biopsy

81. Management
• Dialysis
• Renal Transplantation