medical treatment

1. GENITO URINARY AND RENAL
DISORDERS
1

4. Functions of the Kidney
 Urine formation
• Excretion of waste products
• Regulation of electrolytes
• Regulation of acid–base balance
• Control of water balance
• Control of blood pressure
• Regulation of red blood cell production
• Synthesis of vitamin D to active form
4

5. UTIs
 urinary tract is sterile above the urethra.
Lower UTIs include :
 bacterial cystitis (inflammation of urinary bladder),
 bacterial prostatitis (inflammation of prostate gland),
 bacterial urethritis (inflammation of the urethra)
5

6. UTIs…
Upper UTIs are much less common and include:
 Acute or chronic pyelonephritis (inflammation of
the renal pelvis)
 Interstitial nephritis (inflammation of the kidney),
and
 Renal abscesses
6

7. UTIs …
Several mechanisms maintain the sterility of the
bladder:
 urine flow,
urethero-vesical junction Competence
various antibacterial enzymes and antibodies
Anti-adherent effects mediated by the mucosal
cells of the bladder.
Abnormalities or dysfunctions of these mechanisms
are contributing factors to lower UTIs. 7

8. Pathophysiology UTIs
 Bacteria must gain access to the bladder
• Attach to and colonize the epithelium
• Envade host defense mechanisms, and Initiate
inflammation.
• Most UTIs result from fecal organisms that ascend from the
perineum
8

9. Risk Factors for UTI
 Inability or failure to empty the bladder completely
 Obstructed urinary flow,
 from congenital anomalies,
 urethral strictures, contracture of the bladder neck
 bladder tumors, calculi (stones) in the ureters or
kidneys,
 compression of the ureters, and
 neurologic abnormalities
9

10. UPPER UTI
1. ACUTE PYELONEPHRITIS
 Inflammation of the structures of the kidney:
 the renal pelvis
 renal tubules
 interstitial tissue
 Almost always caused by E.coli
10

11. Acute Pyelo…………………………………cont
 Bacteria reach the bladder by means of the urethra
and ascend to the kidney.
 Although the kidneys receive 20% to 25% of the
cardiac output, bacteria rarely reach the kidneys
from the blood.
 fewer than 3% of cases are due to hematogenous
spread.
11

12. Pyelonephritis is frequently
secondary to uretero-
vesical reflux, in which
an incompetent uretero-
vesical valve allows the
urine to back up (reflux)
into the ureters.
12

13. RISKS OF ACUTEPYELONEPHRITIS…
 Urinary tract obstruction which increases the
susceptibility of the kidneys to infection are:
 Bladder tumors,
 Strictures,
 Benign prostatic hyperplasia, and
 Urinary stones are some of the other causes.
13

14. ETIOLOGY
 Causative microorganisms are usually
 E. coli, Klebsiella,
Proteus, Serratia,
Pseudomonas, Enterococcus, and
If S. aureus is found suspect;
 bacteremic spread from a distant focus (e.g. septic
emboli in infective endocarditis)
 possible multiple intra-renal abscesses
14

15. Clinical Manifestations
 Acutely ill with chills and fever.
 Pyuria, flank pain, and (CVA tenderness) on the
affected side.
 Dysuria and frequency, are common.
enlarged kidneys
 interstitial infiltrations of inflammatory cells.
Abscesses
15

16. Clinical Manifestations…
 Eventually, atrophy and destruction of tubules
and the glomeruli may result.
 When pyelonephritis becomes chronic, the kidneys
become scarred, contracted, and non-functioning.
16

17. Investigations
 Urine dipstick: +ve for leukocytes and nitrites, possible
hematuria.
 Microscopy: WBC in urine , bacteria.
 Gram stain: Gram negative rods, Gram positive cocci
 Culture
 US or a CT scan may be performed to locate any
obstruction in the urinary tract.
17

18. Differential diagnosis
 Acute appendicitis
 Acute cholecystitis
 Acute diverticulitis
 Pancreatitis
 Herpes zoster affecting somatic segments of T12 &
L1
18

19. Complications
 Chronicity
 Bacteraemia or Septicaemia
19

20. Medical Management
 Acute uncomplicated pyelonephritis- outpatients if
they are:
 Not dehydrated,
 Not nausea or vomiting, and
 Not showing signs or symptoms of sepsis.
 A 2-week course of antibiotics
 ciprofloxacin, or a
 third-generation cephalosporin.
20

21. ACUTE GLOMERULONEPHRITIS
 Glomerulo-nephritis is an inflammation of the
glomerular capillaries.
 Acute glomerulo-nephritis is primarily a disease of
children older than 2 years of age
 can also occur at nearly any age.
21

22. Pathophysiology
• group A beta hemolytic streptococcal
infection of the throat preceed 2 to 3 weeks.
• It may also follow impetigo and acute viral
infections
• Antigen-antibody complexes being deposited
in the glomeruli.
22

23. 23

24. Clinical Manifestations
 Hematuria-The urine may appear cola-colored
because of RBCs and protein plugs or casts.
 Proteinuria- (primarily albumin), is due to the
increased permeability
 CVA tenderness.
24

25. Clinical Manifestations
• BUN and serum Creatinine levels may rise
as urine output drops.
• anemia.
• edema and hypertension is noted in 75% of
patients.
25

26. Clinical Manifestations…
 Acute renal failure with oliguria.
 headache
 malaise,
 flank pain
26

27. Assessment and Diagnostic Findings
 The kidneys become large, swollen, and congested
 All renal tissues—glomeruli, tubules, and blood
vessels—are affected to varying degrees.
 Electron microscopy identify nature of the
 immuno-fluorescent lesion.
 A kidney biopsy 27

28. Complications
Hypertension
Encephalopathy
Heart failure
Pulmonary edema 28

29. Management
 Treating symptoms,
 Attempting to preserve kidney function, and
 Treating complications promptly
 If residual streptococcal infection is suspected,
penicillin is the agent of choice.
 Corticosteroids
 immunosuppressant
29

30. Management
Dietary protein is restricted when renal insufficiency
and nitrogen retention (elevated BUN) develop.
Sodium is restricted when the patient has
hypertension, edema, and heart failure.
Loop diuretic medications and antihypertensive
agents may be prescribed to control hypertension.30

31. NEPHROTIC SYNDROME
Nephrotic syndrome is Damage to glomerular
capillary membrane and results in increased
glomerular permeability.
 characterized by the following:
1. Marked increase in protein in the urine
(proteinuria)
2. Decrease in albumin in the blood
(hypoalbuminemia)
31

32. Cont
3. Edema
4. High serum cholesterol and LDL
(hyperlipidemia)
32

33. Pathophysiology
 can occur with almost any intrinsic renal disease or
systemic disease that affects the glomerulus.
 Commonly affect children, but also nephrotic
syndrome does occur in adults, including the
elderly.
33

34. Causes
 chronic glomerulonephritis
 diabetes mellitus with intercapillary
glomerulosclerosis
 renal vein thrombosis.
34

35. 35
Pathophysiology.

36. Clinical Manifestations
• Edema- soft and pitting and most commonly occurs
around : eyes (periorbital)
Also edema of:
 sacrum
• Ankles
• hands
• abdomen (ascites)
• Malaise, headache, irritability, and fatigue, are
common 36

37. Figure 1. Nephrotic edema.

38. Figure 2. Nephrotic edema.

39. Assessment and Diagnostic Findings
• Proteinuria (albumin) exceeding 3 to 3.5 g/day is
sufficient for the diagnosis of nephrotic syndrome.
• Increased WBCs as well as granular and epithelial
casts in the urine.
• A needle biopsy of the kidney may be performed for
histological examination of renal tissue to confirm the
diagnosis. 39

40. Management
The objective of management is to preserve renal
function
 The use of angiotensin-converting enzyme (ACE)
inhibitors in combination with diuretics often
reduces the degree of proteinuria but may take 4 to
6 weeks to be effective
40

41. Management
• low-sodium- to reduce edema.
• Protein intake should be about 0.8 g/day,
with emphasis on high biologic proteins
(dairy products, eggs, meats)
 diet should be low in saturated fats. 41

42. ACUTE RENAL FAILURE
• Acute renal failure (ARF) is a sudden and almost
complete loss of kidney function (decreased GFR)
over a period of hours to days.
 ARF manifests with oliguria, anuria, or normal urine
volume.
 Oliguria (less than 400 mL/day of urine) is the most
common clinical situation seen in ARF.
42

43.  Anuria (less than 50 mL/day of urine) and
normal urine output are not as common.
 patient with ARF experiences rising serum
Creatinine and BUN levels and retention of
other metabolic waste products
(azotemia).
43

44. CATEGORIES OF ARF
Three major categories of conditions cause
ARF:
1. Prerenal
2. Intrarenal
3. Postrenal.
44

45. Category of ARF…
Pre-renal Failure
• Volume depletion resulting from:
 Hemorrhage
 Renal losses (diuretics, osmotic diuresis)
 Gastrointestinal losses (vomiting, diarrhea,
nasogastric suction)
45

46. Intrarenal Failure
 Prolonged renal ischemia resulting from:
 Infectious processes
 Nephrotoxic agents such as:
 Aminoglycoside antibiotics (gentamicin,
tobramycin)
46

47. Cont’d
 Post renal Failure
• Urinary tract obstruction, including:
 Calculi (stones)
 Tumors
 Benign prostatic hyperplasia
 Strictures
 Blood clots
47

48. c/m
The patient may appear:
 critically ill
 lethargic, with
 persistent nausea, vomiting, and diarrhea.
 skin and mucous membranes are dry from
dehydration.
48

49. c/m
 breath may have the odor of urine (uremic
fetor)
 drowsiness, headache, muscle twitching,
and seizures
49

50. Assessment and Diagnostic Findings
 Changes in urine
 Increased BUN and Creatinine levels (Azotemia)
 Hyperkalemia
 Metabolic acidosis 50

51. Medical Management
objectives
 restore normal chemical balance
 prevent complications until repair of renal tissue and
restoration of renal function can take place.
 Any possible cause of damage is identified, treated,
and eliminated.
51

52. Medical Management
 Prerenal azotemia is treated by optimizing renal
perfusion
 postrenal failure is treated by relieving the
obstruction .
 Treatment of intrarenal azotemia is supportive,
with removal of causative agents
 Sodium bicarbonate, dialysis or kidney
replacement. 52

53. 53

54. Urolithiasis
 Urolithiasis refers to stones (calculi) in the urinary
tract.
formed when urinary concentrations of substances
such as;
 calcium oxalate,
 calcium phosphate, and
 uric acid increase.
 The higher PH, the less soluble are calcium and
phosphate, the lower PH, the less soluble are uric
acid and cystine. 54

55. Pathophysiology
Stones can also form when there is a deficiency of
substances that prevent crystallization such as
 citrate,
 magnesium,
 nephrocalcin, and
 uropontin.
 dehydrated patients
 Calculi may be found anywhere from the kidney to
the bladder.
 They vary in size from minute granular deposits, to
as large as an orange. 55

56. 56

57. Pathophysiology
 Certain factors favor the formation of stones,
including
 infection, urinary stasis, and
 periods of immobility-slows renal drainage and
alters calcium metabolism.
 increased calcium concentrations
 About 75% of all renal stones are calcium-
based
57

58. Pathophysiology
Causes of hypercalcemia and hypercalciuria
include:
 Hyperparathyroidism, Renal tubular acidosis,
Cancers
 Excessive intake of vitamin D
 Excessive intake of milk . 58

59. Path…
Uric acid stones (5% to 10% of all stones).
Calcium oxalate: idiopathic hypercalcuria,
hyperoxaluria
Calcium phosphate: mixed stone.
 Due to alkaline urine, primary
hyperparathyroidism.
59

60. Pathophysiology
Cystine stones (1% to 2% of all stones)
occur exclusively in patients with a rare inherited
defect in renal absorption of cystine (an amino
acid).
60

61. Risk factors in development of Urinary Tract Calculi
61
Diet
Large diet of dietary proteins that increase uric excretion
Excessive amounts of tea or fruit juice increases urinary oxalate
level.
Large intake of calcium and oxalate.
Low fluid intake that increase urinary concentration
Lifestyle
Sedentary occupation, immobility

62. Clinical Manifestations
Obstruction, infection, and edema.
 hydrostatic pressure
 distending the renal pelvis and proximal ureters.
Infection (pyelonephritis and cystitis) with;
 chills,
 fever, and
 dysuria. 62

63. Clinical features
 Deep ache in the costovertebral region indicates
stones in the renal pelvis.
 Hematuria
 pyuria
 Acute, excruciating, colicky, wavelike pain, radiating
down the thigh and to the genitalia indicate Stones
lodged in the ureter (ureteral obstruction).
63

64. Cont
 UTI and hematuria.
 urinary retention- If the stone obstructs the
bladder neck.
 sepsis threatening the patient’s life.
64

65. Assessment and Diagnostic Findings
 x-ray
 intravenous urography
 Blood chemistries and a 24-hour urine test for
measurement of:
 Calcium, uric acid, Creatinine, sodium
 Dietary and medication histories
 family history
65

66. Medical Management
The basic goals of management are :
to eradicate the stone,
to determine the stone type,
to prevent nephron destruction,
to control infection, and
to relieve any obstruction that may be present.
 .
66

67. mgt
 relieve the pain until its cause can be
eliminated .
 Opioid analgesics are administered to prevent
shock and syncope that may result from the
excruciating pain
67

68. Medical Management
 Hot baths or moist heat to the flank areas may also
be useful.
 Fluids are encouraged
 Uric Acid Stones: place on a low-purine diet to
reduce the excretion of uric acid in the urine.
68

69. Con’t
Allopurinol (inhibit the conversion of nucleic acids to
uric acid)
 reduce serum uric acid levels and
 urinary uric acid excretion.
Oxalate Stones: For oxalate stones;
 dilute urine is maintained
 intake of oxalate is limited. 69

70. Cont’d
Chemolysis, stone dissolution using infusions of
chemical solutions
 alkylating agents,
 acidifying agents for the purpose of dissolving the
stone.
70

71. Cont
Extracorporeal shock wave lithotripsy (ESWL)
 Electromagnetically generated shock waves are
focused over the area of the renal stone.
 The high-energy dry shock waves pass through
the skin and fragment the stone.
71

72. 72
Extracorporeal shock wave lithotripsy (ESWL

73. SURGICAL MANAGEMENT
Cystoscopy- which is used for removing small renal
stones located close to the bladder.
Ureteroscope- is inserted into the ureter to visualize
the stone.
 The stone is then fragmented or captured and
removed. 73

74. 74

75. Cont
 nephro-lithotomy (incision into the kidney with
removal of the stone)
 A nephrectomy -if the kidney is nonfunctional
secondary to infection or hydronephrosis.
75

76. Hydronephrosis
 is dilation of the renal pelvis and calyces of
one or both kidneys due to an obstruction.
 Pathophysiology
 Obstruction to the normal flow of urine
causes the urine to back up, resulting in
increased pressure in the kidney. 76

77. Pathophysiology…
 The obstruction may be due to :
 a tumor pressing on the ureters
 bands of scar tissue resulting from an abscess or
inflammation near the ureters that pinches it.
77

78. Clinical Manifestations
 flank pain and back.
 If infection is present, dysuria, chills, fever,
tenderness, and pyuria may occur.
 Hematuria.
 If both kidneys are affected, signs and symptoms of
chronic renal failure may develop.
78

79. Medical Management
 The goals of management are:
 to identify and correct the cause of the
obstruction.
to treat infection.
to restore and conserve renal function.
79

80. URETHRITIS
 Urethritis is inflammation of the urethra that
usually an ascending infection and may be
classified as
gonococcal or
nongonococcal.
80

81.  Gonococcal urethritis is caused by N.
gonorrhoeae and is transmitted by sexual
contact.
 In men, inflammation of the urethral
meatus or orifice occurs, with burning on
urination.
81

82. c/m
 A purulent urethral discharge appears 3 to 14 days
(or longer) after sexual exposure,
 periurethritis,
 prostatitis,
 epididymitis, and urethral stricture.
 Sterility may occur as a result of vasoepididymal
obstruction.
82

83. Management
 Ciprofloxacine 500 mg po stat or
 Ceftriaxone 1gm or
 Spectinomycine 2 gm im stat.
 Treating partiner
83

84. Cont’d
Non gonococcal urethritis is usually caused by
C.trachomatis
 Male patients with symptoms usually complain of
mild to severe dysuria and scant to moderate
urethral discharge
 Non gonococcal urethritis requires prompt treatment
with tetracycline or doxycycline.
 Treating partner
84