3. 1. Regulation of the volume of blood by
excretion or conservation of water.
2. Regulation of the electrolyte content of the blood
by the excretion or conservation of minerals.
3. Regulation of the acid-base balance of the blood
by excretion or conservation of ions
4. Regulation of all of the above in tissue fluid.
5. Kidneys
- is to separate urea, mineral salts, toxins
and other waste products from the blood.
- filtering out wastes to be excreted in the urine.
- regulating BP
- regulating an acid-base balance
- stimulating RBC production
6. Ureters
- transports urine from the renal pelvis of the
kidney to which it is attracted, to the bladder.
- pass beneath the urinary bladder, which results
in the bladder compressing the ureters and
hence preventing back-flow of urine when
pressure in the bladder is high during urination.
7. Bladder
- store urine
- expels urine into the urethra (Micturation)
Micturation – involves both voluntary and
involutary muscles.
8. Urethra
- is the passageway through which urine is
discharged from the body
10. 1. Nephrons – functional unit of kidney.
Each kidney is formed of about one
million nephrons.
2. Glomerulus – filters the blood
3. Bowman’s Capsule – is a large double
walled cup. It lies in the renal cortex
4. Tubular Component – necessary
substances are being reabsorbed
11. 1. Loop of Henle – create a concentration gradient
in the medulla of the kidney.
- reabsorb water and important nutrients in the filtrate.
2. Renal Vein – a blood vessel that carries
deoxygenated blood out of the kidneys
3. Renal Artery – supply clean, oxygen-rich blood to
the kidneys
4. Adrenal Gland (Suprarenal Gland) – located on top of
the kidneys and is essential for balancing salt and water
in the body
12. Beginning of the process.
• A process by which the blood courses
through the glomeruli, much of its fluid,
containg both useful chemicals and dissolve
waste materials, soaks out the blood
through membranes where it is filtered and
then flows into Bowman’s capsule.
13. Tubular Reabsorption
• A movement of substances out of the renal
tubules back into the blood capillaries located
around the tubules (peritubular capillaries).
14. • disposing of substances not already in the
filtrate (drugs)
• eliminating undesirable substances that have
been reabsorbed by passive processes (urea
and uric acid)
• ridding the body of excess potassium ions
• controlling pH
15. is the amount of fluid filtered from the blood into
the capsule each minute. Factors governing the
filtration rate at the capillary beds are:
1.total surface area available for filtration
2.filtration membrane permeability
3.net filtration pressure
24. • Kidneys performed as the body’s main Excretory
function by filtering the blood and selectively
reabsorbed those materials that are needed to
maintain a stable internal environment.
• Nephrons is the functional unit of the kidneys.
It is composed by a glomerulus which filters the blood
and the tubular component where necessary
substances are reabsorbed into the the blood stream
and the unneeded materials are secreted into the
tubular filtrate for elimination and urine.
28. Urinary incontinence has been defined by the
international continence society (ICS) as “a condition
in which involuntary loss of urine is a social or
hygienic problem and is objectively demonstrable”.
29.
30.
31. Stress incontinence
Urge incontinence
Overflow incontinence
Reflex incontinence
Functional incontinence
Others
after trauma and surgery
Due to prostrate cancer
32. Urinary incontinence commonly result from many
factors including anatomic defects, physical,
physiological, psychosocial and pharmacological
Anatomic and physiologic incontinence results
from sphincter weakness or damage, urethral
deformity, altered muscle tone at the
urethrovesical junction (Q-tip test) and detrusor
instability
- Q-tip test is for the urethral hyper mobility of the
urethrovesical junction
33. Stress incontinence
- Found most commonly in women with relaxed
pelvic floor muscles (from delivery, use of
instrumentation during vaginal delivery or
multiple pregnancies).
- Female urethra atrophy when estrogen
decreases after menopause.
- Prostate surgery for BPH or prostate cancer.
- Repeated straining, urogenital prolapsed and
congenital weakness.
34. - Surgical interventions may cause bladder
neck damage, with possible permanent
incontinence.
- Hypermobile urethrovesical junction.
36. Major manifestation of urinary incontinence is
involuntarily loss of urine in all types.
1. Stress incontinence
- Leakage in small amounts
- May not be daily
37. - Condition is caused by uncontrolled contraction or
overactivity of detrusor muscle.
- Bladder escapes central inhibition and contracts
reflexively.
- Condition includes CNS disorder (e.g. cerebrovascular
disease , Alzheimer's disease , brain tumor, parkinson’s
disease)
- Bladder disorders (e.g. carcinoma in situ , radiation effect,
cystitis)
- Interference with spinal inhibitory pathways (malignant
growth in spinal cord, spondylosis and the bladder outlet
obstruction)
46. - Disorder is caused by bladder or urethral outlet
obstruction ,( or caused by bladder neck
obstruction , urethral stricture ,pelvic organ
prolapse)
- After surgery such as hemorrhoidectomy,
herniorrhaphy, cystoscopy.
- Neurogenic bladder.
- Drugs can also contribute to incontinence,
specially overflow incontinence, examples are :-
opioidus, tranquilizers, sedatives and hypnotic
agents, alcohols, rapid acting diuretics,
antihistamines, atropine, hypotensive agents,
ganglionic blockers
47. Overflow incontinence
If obstruction in bladder outlet
Over distention
Bladder remains full
Urethra constricts
Completed void is not there (urinary retention)
but due to overflow urine leaks involuntarily (but not completely due to
distention and constriction of urethra)
48. OVERFLOW INCONTINENCE
- Feeling of fullness in bladder
- No sphincter control
- Frequent leakage in small amounts
- Palpable and distended bladder
- feeling of incomplete voiding (as in urinary
retention)
49. - Fistula may occur during pregnancy, after
delivery of baby , as a result of
hysterectomy, or invasive cancer of cervix,
or after radiation therapy.
- Incontinence is found as post operative
complication after transurethral, perineal or
retropubic prostatectomy.
50. Urodynamic examination
- cystometrography
- electromyographic
- urine flow rate (help to identify hypotonic
detrusor or an obstructional or dysfunctional
voiding mechanism)
- Urethral pressure profile (to detect pressure in
urethra in stress incontinence)
- Ultrasonography and catheterization (can detect
the elevated residual urine level)
51. - cystoscopy (for tumors, foreign bodies such a
stones) or structural abnormalities in the bladder
and urethra.
- Q-tip test.
- an excellent diagnostic tool, the bladder diary,
reveals voiding frequency, fluid intake, pattern of
urinary urgency and no. of severity of incontinent
episodes. A seven day diary reveals pattern of
incontinence and may be helpful before a
diagnostic evaluation.
52. Electrical stimulation
Medications
#Anticholenergic agents such as
1. Oxybutynin (Ditropan) and Tolterodine (Detrol):-
Anticholenergic agents work by
- increasing volume in the bladder
- inhibits involuntary contractions
- increase the total bladder capacity
- ditropan : antispasmodic action
53. # Tricyclic antidepressants
1. Imipramine (Tofranil) and Amitriptyline (Elavil)
- Increase the bladder ball relaxation and bladder
capacity.
# Pseudoephedrine (Sudafed)
- a very commonly used drug
- stimulates the alpha receptors
- constricts urethra, or the closer mechanism of
urethra
is increased
54. # Vaginal estrogen (for women)
- enriches genitourinary system with
estrogen receptor leads to good blood
supply to vaginal mucosa.
- prevents atrophy of mucosa.
- maintains elasticity of urethra and ability to
close properly.
55. Monitor fluid intake
Teach kegal exercises
Develop a voiding schedule
Implement biofeedback techniques
Use behavior modification
Explore obstructive devices
Skin care
Recommend counselling
Encourage follow up
56. Use of other incontinence products
Disposable pads
Condom systems
57. Stress incontinence
- pelvic floor muscle exercises e.g., kegal
exercises
- weight loss if patient is obese
- cessation of smoking
- topical estrogen products
- external condom catheters or penile
clamps in men
58. - Treatment of underlying cause
- behavioral interventions including bladder
retraining with urge suppression
- decrease in dietary irritants
- bowel regularity
- pelvic floor muscle exercises
- external condom catheters
- Vaginal estrogen creams
59. - Urinary catheterization to decompress
the bladder
- Intra vaginal device such as a pessary to
sport the prolapse
- intermittent catheterization
60. - treatment of underlying cause
- bladder decompression to prevent urethral
reflux and hydronephrosis
- intermittent self catheterization
- diazepam to relax external sphincter as
prescribed
61. Incontinence after trauma and surgery
- External condom catheter
- penile clamp
- placement of artificial implantable
sphincter
62. Functional incontinence
- Modification of environment or care plan that
facilitate regular, easy access to toilet and
promote patient safety
1. Better lightening
2. Ambulatory assistance
3. Equipment
4. Clothing alterations
5. Timely voiding
6. Different toileting equipment
63. 1. Bladder neck suspension
Restore the normal urethrovesical junction
or lengthen and support the urethra.
2. Implantation of an artificial urinary sphincter
Implantation of an artificial urinary sphincter
may help some clients to achieve
continence.
This procedure is usually avoided until all
other treatments have failed.
64. Maintain adequate urinary drainage
With bladder suspension, preventing
distention is a priority to help in avoiding
excessive pressure on the healing surgical
site
Bladder training program is initiated to help
the client to regain detrusor muscle tone.
Clamp the catheter for lengthening intervals
while urine collects in the bladder, unclamping
it periodically to empty the bladder.
65. If client reports severe pressure,
immediately unclamp the catheter.
If a suprapubic catheter is used, the client
should try to void every two to three hours.
After voiding is attempted, catheter is
drained to measure the residual urine.
66. Urinary incontinence is uncontrolled leakage
of urine.
Approximately 17 million people living in the
united states suffer from urinary incontinence.
Among young adults to middle aged women,
prevalence rate is 30% to 40% and it
increases to 30% to 50% in elderly women.
In contrast urinary incontinence in men tends
to be considerably lower ranging from 1% to
5% in young adult men and increasing 9% to
34% in elderly men
67. Pyelonephritis is the inflammation of renal
pelvis and parenchyma caused by
bacterial infection.
71. Acute pyelonephritis occurs after bacterial
contamination of urethra or
instrumentation such as catheterization
or cystoscopy.
Starts at renal medulla
spreads to cortex
fibrosis and scarring
73. Bacteria enters renal pelvis
Inflammatory response starts
Increased WBC count
Inflammation of pelvis
Edema and swelling of involved tissue
Spreads to papillae
Reach cortex
74. Develops renal abcess
Perinephric abcess
Emphysematous
pyelonephritis
Not treated
Chronic pelonephritis
Decreased no of functioning
nephrons
Replaced by scar tissue
renal failure
Treatment and decreased
inflamation
Fibrosis and scar
development
Calyces become blunted
with scarring of
interstitial tissue
Fibrosis and altered
tubular reabsorption and
secretion
Decreased renal function
76. Frequent urination
Headache
Symptoms subside after few days except
bacteruria
Acute pyelonephritis is Characterized by
-enlarged kidneys
-focal parenchymal abcess
-accumulation of polymorphonuclear
leukocytes around and in tubules
78. Therapeutic aims
Eliminating the pathogenic organisms
with appropriate antibiotics as identified
by urine culture and sensitivity study
Removing component contributing to
decreased host resistance
79. Mild symptoms
Short antibiotic course
Oral antibiotics for 10-14 days
Fluid intake of 3000ml/day
Follow up urine cultures
Severe Symptoms
Hospitalization
Parenteral antibiotics
Fluid intake 3000ml/day
Follow up urine cultures after discharge
80. Dietary alterations e.g for calculi
-Reduce calcium
-Reduce oxalates
for UTI
-acid ash diet
82. Chronic pyelonephritis ( Chronic interstitial
nephritis) is the result of not only acute
pyelonephritis but end result of long
standing UTI with recurrence, relapses of
infections (Slowly ,progressive disease)
83. Chronic obstruction
Long standing UTI
Reflux
Chronic disorders
Associated with recurrent acute attacks
84. H/O acute infection progressing to
chronic renal insufficiency
No specific symptoms of its own
Frequently diagnosed incidently when
client shows HTN or its complications
Chronic PN progresses with other acute
infections
85. Lab studies shows :
-azotemia
-pyuria
-anemia
-acidosis
-proteinuria
Renal biopsy
IVP intravenous pylogram {kind of x ray of urinary
tract}
USG
CT scan
86. Focus is on preventing further renal
damage
Treatment
Appropriate antibiotics
-orally for 2-3 wks
-parenterally for 3-
5days
Control HTN with antihypertensives
87. Nursing Assessment:
History
-present history
-past history
-family history
-social and personal history
Physical examination
Urinalysis
Blood studies
Urine culture and sensitivity
89. Clinical problem Nursing
Diagnosis
Nursing
Intervention
Flank pain Altered comfort ,
flank pain R/T
inflammation and
tissue trauma
-Palpate abdomen
and flank to
identify painful
area
-Position client
for comfort
-Administer
analgesics as
ordered
-Antibiotic may
control
inflammation and
90. Clinical problem Nursing Diagnosis Nursing
Intervention
Altered urinary
elimination R/T
Frequency,
Dysuria
Frequency,
dysuria
-Explain the client
that why it is
-Give fluids
3000ml/day
-Administer I/V
fluids
-Obtain urine
culture and
sensitivity
-Administer
antibiotics
92. Potential for
reinfection
Potential for
reinfection R/T
knowledge deficit
regarding
prevention of
recurrence, S/S
-Instruct client about
preventive measures
Fluids 3000ml/day
Medications
Follow up
Hygiene
Empty bladder before
and after intercourse
Void when urge occurs
Avoid bath salts, sprays
Observe for changes
96. Acute Kidney Injury (AKI), previously called acute
renal failure (ARF) is the rapid breakdown of renal
(kidney) function that occurs when high levels of uremic
toxins (waste products of the body's metabolism)
accumulate in the blood.
ARF occurs when the kidneys are unable to excrete
(discharge) the daily load of toxins in the urine.
Acute renal failure is a syndrome defined by a sudden loss
of renal function over several hours to several days.
97. It is characterized by:
Oliguria
Body water and body fluids disturbances
Electrolyte dearangement
98. India's national CKD registry organized under the
auspices of Indian Society of Nephrology and housed
in Kidney Institute at Nadiad has given data from
45,885 subjects admitted to 166 kidney centers in
India upto January 2010.
ARF affects approximately 1% of patients on
admission to the hospital, 2% to 5% during the
hospital stay, and 4% to 15% after cardiopulmonary
bypass surgery.
101. Prerenal causes are those that interfere with renal
perfusion. The kidneys depend on adequate delivery
of blood to be filtered by glomerulus.
Reduced renal blood flow
Lowers the GFR
ARF
105. It involves parenchymal changes caused by disease
or nephrotoxic substances. Intrinsic ARF accounts
for approximately 40% of the cases of acute renal
failure.
The causes can be classified as follows:
Vascular disease
◦ Glomerulonephritis (GN) and vasculitis
(inflammation of blood vessels)
◦ Renal artery obstruction (atherosclerosis,
thrombosis)
106. • Renal vein obstruction (thrombosis)
• Low blood platelet and red blood cell counts
Diseases of tubules and interstitium (space between
parts of tissue)
• Amyloidosis (deposition of proteins in kidney tissues)
• Interstitial nephritis (associated with allergy or
infection)
Acute tubular necrosis (70%)
• Ischemia (lack of blood flow to an organ)
• Toxins
107. Postrenal ARF is caused by an acute obstruction that
affects the normal flow of urine out of both kidneys.
Blockage/ Obstruction
Causes pressure to build in all of the renal nephrons
(tubular filtering units that produce urine)
Excessive fluid pressure causes the nephrons to shut
down
108. The degree of renal failure corresponds directly with
the degree of obstruction
Postrenal ARF is seen most often in elderly men with
enlarged prostate glands that obstruct the normal flow
of urine.
109. Bladder outlet obstruction due to an enlarged
prostate gland or bladder stone
Ureteric stones
Neurogenic bladder (overdistended
bladder caused by inability of the
bladder to empty)
Tubule obstruction
Renal injury
110.
111. Based on the amount of urine that is excreted over a
24-hour period, patients with ARF are separated into
two groups:
Oliguric: patients who excrete less than 400
milliliters per day.
Nonoliguric: patients who excrete
more than 400 milliliters per day.
112. Onset or initiating phase: It covers the period
from the precipitating event to the development
of renal manifestations.
Oliguric-anuric phase: It lasts for 1-8weeks.
Dialysis may be required in this phase.
Diuretic phase: A gradual or abrupt return to
GFR and leveling of BUN. U/O may be 1000-
2000ml which leads to dehydration.(25% of
deaths occur in this phase)
113. Recovery phase(3-12months): During this time
the client returns to an activity level similar to that
before the onset of the illness. Mild tubular
abnormalities, glycosuria, decreased concentrating
ability may continue for years and client is at the
risk for fluid and electrolyte imbalance.
114. 1. Decreased blood flow
2. Decreased permeability of glomerular
basement membrane
3. Tubular obstruction
4. Back leak of GF through damaged epithelial
cell tubules
115. Normal auto regulation
In decreased renal blood flow
Nephrons autoregulates Blood flow through
glomerulus and pressure
Efferent arteriole vasoconstriction
Decreases blood flow out of glomerulus
Maintains glomerular pressure sufficient for
filtration
116. renal blood flow
renal perfusion to cortex <90% and medulla <10%
Ratio of hyperperfusion altered
Decreased cortical perfusion
Triggers renin angiotensin system to inc blood flow
rate of perfusion in afferent vessels triggers an
increase renin
117. Renin forms angiotensin II
More reduced blood flow
Increased ischemia
Stimulates prostaglandins synthesis for vasodilation
Compensates Inc blood flow Prolongs hypoperfusion
Decreased prostaglandin inhibition
Renal ischemia
Tubular necrosis
Decreased GFR
Renal failure
118.
119. U/O: 2l/day (dilute with low specific gravity)
Hypertension and tachypnea
Extracellular fluid depletion: (dry mucus
membranes, poor skin turgor, orthostatic
hypotension)
Azotemia
120. U/O: Less than 400ml/day
Kidney loses conc. ability
121. Prerenal failure:
• High specific gravity and osmolarity of urine and there is no
or little proteinuria,
• BUN: Creatinine ratio is significantly elevated b/w 10:1 and
40:1.
Inrarenal & Postrenal failure:
• Edema, weight gain, hemoptysis, weakness, anemia, HTN,
hematuria.
• Urine has high specific gravity, high Na concentration with
proteinuria.
• Elevated levels of serum creatinine, potassium.
122.
123. • History and Physical examination
• Urinalysis
• Urine culture
• Urine Specific Gravity
Prerenal Failure: Specific Gravity >1.020
Intrarenal Failure: Specific Gravity 1.010 - 1.020
• ECG: to check the effects of hypo and
hyperkalemia.
• X-ray(KUB)
124. - RFT (renal function tests) Serum creatinine, Na, BUN levels.
Criteria for acute renal failure
Serum Creatinine rises >0.3 on 2 contiguous days or
Serum Creatinine rises >0.5 mg/dl or
Serum Creatinine rises >50% above baseline or
Calculated GFR falls >50% below baseline
- Renal biopsy
- Hemogram- Hb, TLC, DLC, Platelet Count
- ABGs- Metabolic Acidosis
- Electrolytes – Na, K, Cal, Mg, Ph, Ca
127. A history of chronic symptoms of
fatigue,
weight loss,
anorexia,
pruritis
Exposure to heavy metals
Nephrotoxic drug ingestion
History of trauma
Blood loss or transfusions
Evidence of connective tissue disorders or autoimmune
diseases
Urine output history can be useful.
128. Past medical history
Hypertension
Congestive cardiac failure
Diabetes
Multiple myeloma
Chronic infection
Myeloproliferative disorder
129. Consensus criteria (RIFLE for the diagnosis of ARF
are:
Risk: serum creatinine increased 1.5 times OR urine
production of <0.5 ml/kg body weight for 6 hours
Injury: creatinine 2.0 times OR urine production
<0.5 ml/kg for 12 h
Failure: creatinine 3.0 times or urine output below
0.3 ml/kg for 24 h
130. Loss: persistent ARF or complete loss of kidney
function for more than four weeks
End-stage Renal Disease: complete loss of kidney
function for more than three months
136. Objectives
Preventing and treating effects
Attaining and maintaining adequate hydration
Prevention of contributing factors
Prompt recognition and restoration of optimal
renal function
137. Eliminate the cause
Hemodynamic support
Respiratory support
Fluid management
Electrolyte management
Medication dose adjustment
Dialysis
138. Maintenance of fluid and electrolyte balance on the
basis of output and wt
Limit Fluid Intake to Urine Output + 300-500 ml/day:
Usually it is calculated on the basis of previous day’s
U/O + an amount of 400ml.
Monitor weight daily
Hyponatremia - Proper fluid replacement(limit Na
intake to 2g/day)
Hyperphosphatemia
• Administration of aluminum hydroxide or other phosphate
binders
• Low phosphorus diet
Hypocalcemia
• Calcium & Vitamin D supplements
139. Hypertension
•Fluid and Sodium Restrictions
•Diuretic (Lasix or Mannitol)
•Anti- hypertensive's (Propanolol)
Hyperkalemia
•Administration of calcium- it antagonizes membrane
actions
•Cation exchange resins (K-bind, Kayexalate)
•Sorbitol – Osmotic cathartic to induce diarrhea to excrete
potassium
•Low potassium diet
•Dextrose-insulin infusion
•Dialysis
•Dietary Potassium intake <50 meq per day
140. Metabolic Acidosis
•Administration of Sodium bicarbonate, sodium
lactate, and sodium acetate can be given
Anemia
•Administration of eptoein alfa, folic acid, blood
transfusions
Infections
•Antibiotic
Nutritional Status
•High Calorie, Low-Protein, Sodium, magnesium,
phosphorus, potassium limited
141. Hypermagnesemia
Avoid dark green vegetables and whole grains.
Treat seizures
• Phenytoin
• Phenobarbitone
Prevention of pericarditis
• Medications
steroids
NSAIDs
144. Access : Veno-venous
It is a mode of renal replacement therapy for
hemodynamically unstable, fluid overloaded, catabolic
septic patients especially in the critical care /intensive care
unit setting.
The techniques most commonly used are slow continuous
hemodialysis and hemodiafiltration.
These patients having various co-morbid conditions are on
mechanical ventilation and various life supporting
modalities which do not merit the dialysis procedure to be
carried out in the routine dialysis set up.
145. These patients require continuous clearance of waste
produced due to ongoing illnesses and an adequate
potential for infusion of nutritional and inotropic agents
for sustenance of vital parameters.
146. Presence of marked azotemia
Fluid overload
Persistent oliguria
Hyperkalemia
Refractory pulmonary edema
Pericarditis
Serial rise in blood urea and serum creatinine.
ARF with cardiovascular instability
ARF with septicemia
ARF with septicemia and ARDS.
ARF with cerebral edema
Systemic inflammatory response syndrome
147. 1. CRRT by its lower rate of fluid removal can lead to
steady state fluid equilibrium in hemodynamically
unstable, critically ill patients with associated
comorbid conditions eg. M.I, ARDS, septicemia,
bleeding disorders.
2. It provides excellent control of azotemia, electrolytes
and acid base balance.
3. It is efficacious in removing fluid in special
circumstances – post surgery, pulmonary edema;
ARDS etc.
148. 4. CRRT can help in administration of parenteral
nutrition and obligatory I.V medications like pressors
& inotropes by creating an unlimited space by virtue
of continuous ultrafiltration.
5. Hemofiltration modality is effective in lowering
intracranial tension v/s routine intermittent
hemodialysis which can sometimes raise intracranial
tension.
6. Proinflammtory mediators of inflammation are also
shown to have been removed by this modality eg.IL-
1, IL-6, IL-8, TNF-a.
149. This mode of therapy requires regular
monitoring of hemodynamic status and fluid
balance (ultrafiltration rate, replacement fluid);
regular infusion of dialysate; continuous
anticoagulation; ongoing alarms and an
expensive mode of therapy above all.
151. 1. Fluid volume excess R/T decreased GFR
manifested by edema/weight gain
2. Altered nutrition :less than body requirement
R/T high catabolic state
3. Risk for infection R/T lowered resistance
4. Risk for injury R/T weakness, confusion,
postural hypotension
5. Knowledge deficit about the disease condition
152. Expected outcomes: Patient will be having no fluid
retention as evidenced by no or reduced edema, HR
within limits and stable BP.
Interventions:
-Record I/O, Acid base balance, electrolyte levels
-Measure weight, B.P, Auscultate lungs
-Assess for peripheral edema, decrease in Urine output,
increase in B.P, hyperkalemia
-Assess respiratory rate
153. - -Assess for the need for dialysis
-Inspect skin for breakdown
- Raise extremities
-Treat hyperkalemia by avoiding foods
containing K+, administering kayexalate (Ion
exchange resin)
-Look for S/S of hyperkalemia (muscle weakness,
arrhythmia, flaccidity)
154. Expected outcome: Patient will be having improved
nutrition pattern as evidenced by improved hemoglobin
levels, decreased fatigue and weakness.
Interventions :
- Encourage high carbohydrate, high fat diet
- Restrict potassium and proteins
- Serve in an attractive manner
- Consider likes and dislikes
- Consult dietician
155. Expected outcome: Patient will have reduced chances
of infection as evidenced by normal Hemogram, stable
vital signs.
Interventions:
- Use aseaptic technique during all treatments especially
with invasive lines and catheters
- Relieve pruritis by using superfatted soap and
antipruritic medications
- Maintain pulmonary hygiene
156. Expected outcome: patient will have increased
awareness regarding diet, medication, rest, follow-up.
- Teach the pt and family about:
cause and problems with recurrent failure
Identification of preventable environment or health
factors
prescribed medications
prescribed dietary regimen
Risk for hyperkalemia and reportable S/S
S/S of infection and methods of prevention
Follow-up
157.
158. Chronic kidney disease (CKD) is a
worldwide public health problem. It is
recognized as a common condition that is
associated with an increased risk of
cardiovascular disease and chronic renal
failure (CRF).
159. Chronic renal failure is a
progressive, irreversible
deterioration in renal
failure in which the body’s
ability to maintain
metabolic and fluid and
electrolyte balance fails,
resulting in uremia or
azotemia ( retention of
urea and other nitrogenous
wastes in the blood).
160. The Kidney Disease Outcomes Quality
Initiative (K/DOQI) of the National Kidney
Foundation (NKF) defines Chronic kidney
disease as either kidney damage or a
decreased Glomerular filtration rate (GFR)
of less than 60 ml/min for 3 or more
months.
161. Causes of chronic kidney disease include the
following:
Vascular disease
Glomerular disease (primary or secondary)
Tubulointerstitial disease
Urinary tract obstruction
163. Renal vein thrombosis primary
Glomerular disease
o Membranous nephropathy
o Immunoglobulin A (IgA)
nephropathy
o Focal and segmental
glomerulosclerosis (FSGS)
o Minimal change disease
o Membranoproliferative
glomerulonephritis
164. Secondary glomerulus
disease
o Diabetes mellitus
o Systemiclupus erythematus
o Rheumatoid arthritis
o Hepatitis B and C
o Syphilis
o Human immunodeficiency
virus (HIV)
o Parasitic infection
165.
166. Causes of Tubulointerstitial disease
o Drugs (e.g. allopurinol)
o Infection (viral, bacterial, parasitic)
o Chronic Hypokalemia
o Chronic hypercalcemia
o Polycystic kidneys
167. Urinary tract obstruction
o Urolithiasis
o Benign prostatic hypertrophy
o Tumours
o Urethral stricture
o Neurogenic bladder
168. Total Glomerular filtration rate decreases (
reduced clearance)
Serum Creatinine and nitrogen level
increase
Nephrons works harder to eliminate
Creatinine and nitrogen
169. Decreased urine concentration results
Urine production increases
Tubules decrease reabsorption of electrolyte
Sodium loss may occur( can result in polyuria)
Renal damage progresses
170. In 2002, K/DOQI published its
classification of the stages of chronic
kidney disease, as follows:
Stage 1 :- Slightly diminished function;
kidney damage with normal or relatively
high GFR (≥90 ml/min). Kidney damage is
defined as pathological abnormalities or
markers of damage, including
abnormalities in blood or urine test or
imaging studies.
171. Stage 2 :- Mild reduction in GFR (60-89
mL/min) with kidney damage. Kidney
damage is defined as pathological
abnormalities or markers of damage,
including abnormalities in blood or urine
test or imaging studies.
172. Stage 3 :-
Moderate reduction in GFR (30-59
mL/min).
British guidelines distinguish between
stage 3A (GFR 45-59) and stage 3B (GFR
30-44) for purposes of screening and
referral.
Stage 4 :- Severe reduction in GFR (15-29
mL/min) Preparation for renal replacement
therapy
173. Stage 5 :- Established kidney failure (GFR
<15 mL/min, or permanent renal
replacement therapy.
174. Stage 1:- Reduced renal reserve,
Characterized by a 40% to 75% loss of
nephro function.
The patient usually does not have
symptoms because the remaining
nephrons are able to carry out the normal
functions of the kidney.
175. Stage 2:- Renal insufficiency
It occurs when 75% to 90% of nephrons
function is lost.
At this point, the serum Creatinine and
blood urea nitrogen rise, the kidney losses
its ability to concentrate urine and anemia
develops.
The patient may reports polyuria and
nocturia.
176. Stage 3:- End stage renal disease
The final stage of CRF occurs when there is
less than 10% nephron function remaining.
All of the normal regulatory, excretory and
hormonal function of the kidney are severely
impaired.
ESRD is evidenced by elevated by the
Creatinine and blood urea nitrogen levels as
well as electrolyte imbalances.
Once the patient reaches this point, dialysis is
usually indicated.
177. Neurologic:-
Weakness and fatigue
Confusion
Inability to concentrate
Disorientation
Tremors
Asterixis
Restless of legs
Burning of soles of feet
Behavior changes
178. Integumentory:-
Gray bronze skin color
Dry flaky skin( atrophy of the sweat gland)
Pruritis
Ecchymosis
Purpura
Thin brittle nails
Thinning hairs
180. Pulmonary:-
Crackles, thick, tenacious sputum
Depressed cough reflex
Pleuritic pain
Shortness of breath
Tachypnea
Kussmaul type respiration
Uremic pneumonitis
181. Gastrointestinal:-
Ammonia odor to breath
Mouth ulcerations and bleeding
Anorexia, nausea and vomiting
Hiccups
Constipation or diarrhea
Bleeding from gastrointestinal tract
185. High levels of urea in the blood, which can result
in:
Vomiting and/or diarrhoea which may lead
to dehydration
Nausea Weight loss
Nocturnal urination
More frequent urination, or in greater
amounts than usual with pale urine, Less
frequent urination, or in smaller amounts
than usual, with dark coloured urine.
186. A build up of phosphates in the blood that
diseased kidneys cannot filter out may
cause:
Itching
Bone damage
Non-union in broken bones
Muscle cramps (caused by low levels of
calcium which can cause hypocalcaemia)
187. A build up of potassium in the blood that
diseased kidneys cannot filter out (called
Hyperkalemia) may cause:
Abnormal heart rhythms
Muscle paralysis
188. Failure of kidneys to remove excess fluid may
cause:
Swelling of the legs, ankles, feet, face
and/or hands
Shortness of breath due to extra fluid on
the lungs (may also be caused by
anaemia)
189. Healthy kidneys produce the hormone
erythropoietin which stimulates the bone
marrow to make oxygen-carrying red blood
cells.
As the kidneys fail, they produce less
erythropoietin, resulting in decreased
production of red blood cells to replace the
natural breakdown of old red blood cells. As a
result, the blood carries less haemoglobin, a
condition known as anaemia. This can result
in:
191. Other symptoms include:
Appetite loss
A bad taste in the mouth
Difficulty sleeping
Darkening of the skin
Excess protein in the blood
192. Urinalysis:- Decreased GFR can be
detected by obtaining a 24 hours urine
analysis for Creatinine clearance.
As GFR decreases, the Creatinine
clearance value decreases, where as the
serum Creatinine value increase.
193. Serum Sodium and
Potassium level:- The
kidney is unable to
concentrate or dilute the
urine normally in ESRD.
Some patient retain
sodium, potassium and
water, increasing the risk
for edema, congestive
heart failure and
hypertension.
194. pH:- With advanced renal disease,
metabolic acidosis occurs because the
kidney is unable to excrete increased
loads of acids.
195. Complete blood Count:- Anemia develops
as a result of inadequate erythropoietin
production, the short life span of RBCs,
nutritional deficiencies and the patient
ability to bleed.
In renal failure, erythropoietin production
decreases and profound anemia results,
producing fatigue, angina and shortness of
breath.
196. Serum calcium and Phosphorus:- With in
the decrease in the GFR, there is an
increase in the serum phosphate level and
a reciprocal or corresponding decrease in
the serum calcium level.
197. KUB is usually done first to determine
whether there is a problem with the
structure of the renal system.
An IVP and CT scan can be done to
assess renal structure and function.
Renal angiography may also be done
to assess the blood supply to and
through the kidneys.
Renal ultrasonography is useful to
screen for hydronephrosis which may
be not observed in early obstruction.
199. The goal of management
is to maintain kidney
function and homeostasis
for as long as possible.
All the factors that
contribute to ESRD and
all factors that are
reversible ( e.g.
obstruction) are identified
and treated.
200. Antacid:- Hyperphosphatemia and
hypocalcemia are treated with aluminum
based antacids that binds dietary phosphorus
in the gastrointestinal tract.
Phosphate-Lowering Agents
Dietary phosphate binders promote the
binding of phosphate, typically with calcium,
to reduce Hyperphosphatemia.
Calcium acetate
Calcium carbonate
Calcitriol
201. Antihypertensive and cardiovascular agents:-
Hypertension is managed by intravascular
volume control and a variety of
antihypertensive medications.
Congestive heart failure and pulmonary
edema may also require treatment with fluid
restriction.
Low sodium diets, diuretics, inotropic agents
such as digitalis or dobutamine and dialysis.
202. Anticonvulsants:- Intravenous diazepam or
phenytoin is usually administered to
control seizures.
Erythropoietin:- Anemia associated with
CRF is treated with recombinant human
erythropoietin ( Epogen).
It is administered subcutaneously three
times a week for the Hematocrit to rise.
204. Nutritional therapy:- Careful regulation of
protein intake.
Fluid intake to balance fluid losses.
Sodium intake to balance sodium losses.
Restriction of potassium.
Adequate calorie intake and vitamin
supplementation must be ensured.
The allowed protein must be of high
biologic value.
205. Dialysis is a process for removing waste and
excess water from the blood, and is primarily used
to provide an artificial replacement for lost kidney
function in people with renal failure.
Dialysis may be used for those with an acute
disturbance in kidney function (acute kidney injury)
, previously acute renal failure) or for those with
progressive but chronically worsening kidney
function–a state known as chronic kidney disease
stage 5 (previously chronic renal failure or end-
stage kidney disease).
206. The latter form may develop over months
or years, but in contrast to acute kidney
injury is not usually reversible, and dialysis
is regarded as a "holding measure" until a
renal transplant can be performed, or
sometimes as the only supportive measure
in those for whom a transplant would be
inappropriate.
207. It may also be used to treat the
patients with intractable ( not
responsive to treatment) edema,
hepatic coma, Hyperkalemia,
hypercalcemia, hypertension and
uremia.
It is usually initiated when the patient
cannot maintain a reasonable
lifestyle with conservative treatment.
208.
209. A different dialysis technique, continuous
ambulatory peritoneal dialysis (CAPD),
makes use of the fact that the peritoneum
(the lining of the abdominal cavity) is a
differentially permeable membrane. A
plastic bag containing dialysis fluid is
attached to the patient's abdominal cavity..
210. After about 30 minutes, the fluid is withdrawn
into the bag and discarded. This process is
repeated about three times a day. This type of
dialysis is much more convenient but poses the
threat of peritonitis, should bacteria enter the
body cavity with the dialysis fluid
211.
212. Kidney transplantation, the surgical
implantation of a human kidney from one
person to another , is performed for clients
with irreversible kidney failure.
It involves transplanting a kidney from a
living donor or human cadaver to a
recipient who has ESRD.
213. Patients with chronic kidney disease should
be educated about the following:
Importance of compliance with secondary
preventive measures
Natural disease progression
Prescribed medications (highlighting their
potential benefits and adverse effects)
Avoidance of nephrotoxins
Diet
Renal replacement modalities, including
peritoneal dialysis, hemodialysis, and
transplantation
Permanent vascular access options for
hemodialysis
214. Nursing Diagnosis:- Fluid volume excess
related to decreased urine output, dietary
excesses and retention of sodium and water.
Intervention:- Assess fluid status.
Daily weight.
Intake and output balance.
Skin turgor and presence of edema.
Distention of neck veins
Blood pressure, pulse rate and rhythm
Respiratory rate and effort
215. Limit fluid intake to prescribed volume.
Identify potential sources of fluid:
Medications and fluids used to take
medications : oral and intravenous
Explain to patient and family rationale for
restriction.
Provide or encourage frequent oral
hygiene.
216. Nursing diagnosis:- Altered nutrition; less
than body requirements related to
anorexia, nausea, vomiting, dietary
restrictions.
Interventions:- Assess nutritional status:
Weight changes.
Anthropometric measures
Laboratory values ( serum electrolyte,
BUN, Creatinine and iron level)
217. Assess patient’s nutritional dietary pattern.
Diet history
Food preferences
Calorie counts
Assess for factors contributing to altered
nutritional intake
Anorexia, nausea and vomiting
Depression
Lack of understanding of dietary restrictions
218. Provide patient’s food preferences with in
dietary restrictions.
Promote intake of high biologic value protein
foods: eggs, diary products, meats.
Encourage high-calorie, low protein, low
sodium and low potassium snacks between
meals.
Alter schedule of medications so that they are
not given immediately before meals.
219. Explain rationale for dietary restrictions
and relationships to kidney disease and
increased urea and Creatinine levels.
Provide written list of foods allowed and
suggestions for improving their taste
without use of sodium and potassium.
Provide pleasant surroundings at meal
times.
Weigh patient daily.
220. Nursing Diagnosis:- Knowledge deficit
regarding condition and treatment.
Intervention:- Assess understanding of cause
of renal failure, consequences of renal failure,
and its treatment:
Cause of patient’s renal failure.
Meaning of renal failure.
Understanding of renal function.
Relationship of fluid and dietary restrictions to
renal failure.
Rationale for treatment.
221. Provide explanation of renal function and
consequences of renal failure at patient’s
level of understanding and guided by
patient’s readiness to learn.
Assist patient to identify ways to
incorporate changes related to illness and
its treatment into lifestyle.
Provide oral and written information as
appropriate about:
222. Renal function and failure.
Fluid and dietary restrictions
Medications
Follow up schedule
Community resources
Treatment options
223. Nursing Diagnosis:- Activity intolerance
related to fatigue, anemia, retention of
waste products and dialysis procedure
Intervention:- Assess factors contributing
to fatigue:
Anemia
Fluid and electrolyte imbalances
Retention of waste products
Depression
224. Promote independence in self care
activities as tolerated ;assit if fatigued.
Encourage alternating activity with rest.
Encourage patient to rest after dialysis
treatments.
225.
226. Acute tubular necrosis is a kidney disorder
involving damage to the tubule cells of the
kidneys, resulting in Acute Kidney Failure
(AFI).
227. Acute tubular necrosis or (ATN) is a
medical condition involving the death of
tubular cells that form the tubule that
transports urine to the ureters while
reabsorbing 99% of the water (and highly
concentrating the salts and metabolic
byproducts). Tubular cells continually
replace themselves and if the cause of
ATN is removed then recovery is likely.
228. Acute Kidney Injury (AKI) is observed in
about 5% of all hospital admissions and in
up to 30% of patients admitted to the
intensive care unit (ICU). ATN is the most
common cause of AKI in the renal
category, and the second most common
cause of all categories of AKI in
hospitalized patients, with only prerenal
azotemia occurring more frequently.
230. Toxic ATN can be caused by:
Free hemoglobin or Myoglobin
Medication such as antibiotics such as
aminoglycoside
Cytotoxic drugs such as Cisplatin
Intoxication (ethylene glycol)
231. Toxic ATN is characterized by:
Proximal tubular epithelium necrosis due to
a toxic substance.
Necrotic cells fall into the tubule lumen,
obliterating it, and determining acute renal
failure.
Basement membrane is intact, so the
tubular epithelium regeneration is
possible.
Glomeruli are not affected.
232. Ischemic ATN can be caused :
When the kidneys are not sufficiently
perfused for a long period of time
(e.g. renal artery stenosis, shock).
Hypoperfusion can also be caused by
embolism of the renal arteries.
Ischemic ATN specifically causes skip
lesions through the tubules.
233. Blood transfusion reaction.
Injury or trauma that damages the
muscles.
Recent major surgery.
Septic shock or other forms of shock.
Severe low blood pressure (hypotension)
that lasts longer than 30 minutes.
234. Liver disease and kidney damage caused
by diabetes (diabetic nephropathy) may
make a person more susceptible to the
condition.
Exposure to medications that are toxic to
the kidneys (such as Aminoglycoside
antibiotics)
Antifungal agents (such as Amphotericin)
Dye used for X-Ray studies.
235. Causes of ischemic acute tubular necrosis:
Hypovolemic states: hemorrhage, volume
depletion from gastrointestinal (GI) or renal
losses, burns, fluid sequestration.
Low cardiac output states: heart failure
and other diseases of myocardium,
valvulopathy, arrhythmia, pericardial
diseases, tamponade.
Systemic Vasodilation: sepsis,
anaphylaxis.
245. Symptoms of acute kidney failure may also
be present.
Incresed BUN and serum creatinine levels.
Fractional excretion of sodium and of urea
may be relatively high.
Presence of casts, kidney tubular cells,
and red blood cells in urinalysis.
246. Urine sodium may be high.
Urine specific gravity and osmolarity
decreased indicating dilute urine.
247. The degree of acute kidney injury (AKI) is
determined using the “RIFLE”
R : Risk of renal dysfunction,
I : Injury to the kidney
F: Failure
L: Loss of kidney function
E : End-stage renal disease
251. In most people, acute tubular necrosis is
reversible. The goal of treatment is to
prevent life-threatening complications of
acute kidney failure.
Treatment focuses on preventing the excess
build-up of fluids and wastes, while
allowing the kidneys to heal. Patents
should be closely monitored for
deterioration of kidney function.
253. Correction of oliguria, which may increase
due to the use of diuretics.
Fluid restriction: intake equals to output
considering the sensible loss also.
Restricting the substances normally
removed by Kidney like proteins, sodium,
potassium etc.
254. The duration of symptoms varies. The
decreased urine output phase may last
from a few days to 6 weeks or more. This
is occasionally followed by a period of high
urine output, where the healed and newly
functioning kidneys try to clear the body of
fluid and wastes.
255. One or two days after urine output rises,
symptoms reduce and laboratory values
begin to return to normal.
257. Altered consciousness related to
accumulation of uremic toxins.
Fluid and electrolyte imbalance related to
sodium and water retention.
Altered nutrition less than body
requirement related to nausea and
vomiting.
knowledge deficit related to diseased
condition and its management.
258.
259. Glomerulonephritis is a type of kidney
disease that involves the glomeruli.
During glomerulonephritis, the glomeruli
become inflamed and impair the kidney's
ability to filter urine.
260. The glomeruli are very small, important
structures in the kidneys that supply blood
flow to the small units in the kidneys that
filter urine, called the nephrons.
261.
262. Glomerulonephritis, also known as
glomerular nephritis, abbreviated GN, is
a renal disease characterized by
inflammation of the glomeruli, or small
blood vessels in the kidneys
263. GN is a proliferative immunologic non
bacterial inflammation of the glomerular
structure due to antigen – antibody
reaction.
264.
265.
266. 1 Thin Basement Membrane Disease
2 Non Proliferative GN
Minimal change GN
Focal Segmental Glomerulosclerosis (FSGS)
Membranous glomerulonephritis
3 Proliferative
IgA nephropathy (Berger's disease)
Henoch-Schönlein purpura
Post-infectious
Membranoproliferative/mesangiocapillary GN
Rapidly progressive glomerulonephritis
267. it is an autosomal dominant inherited
disease characterised by thin glomerular
basement membranes on electron
microscopy.
268. This is characterised by low numbers of
cells (lack of hypercellularity) in the
glomeruli. They usually cause nephrotic
syndrome. This includes the following
types:
1. Minimal change GN
2. Focal Segmental Glomerulosclerosis (FSGS)
3. Membranous glomerulonephritis
269. This form of GN causes 80% of nephrotic
syndrome in children, but only 20% in adults.
There is fusion of podocytes (supportive cells
in the glomerulus).
Rx: Treatment consists of supportive care for
the massive fluid accumulation in the patients
body (oedema) and as well as steroids to halt
the disease process (typically Prednisone 1
mg/kg).
270. Only certain foci of glomeruli within the kidney
are affected, and then only a segment of an
individual glomerulus.
The pathological lesion is sclerosis (fibrosis)
within the glomerulus and hyalinisation of the
feeding arterioles, but no increase in the number
of cells (hence non-proliferative).
Rx: Steroids are often tried but not shown to be
effective. 50% of people with FSGS continue to
have progressive deterioration of kidney
function, ending in renal failure.
271. MGN is characterized by a thickened glomerular
basement membrane without a hypercellular
glomerulus.
The basement membrane may completely
surround the granular deposits, forming a "spike
and dome" pattern.
Prognosis follows the rule of thirds: one-third
remain with MGN indefinitely, one-third remit, and
one-third progress to end-stage renal failure .
As the glomerulonephritis progresses, the tubules
of the kidney become infected, leading to atrophy
and hyalinisation. The kidney appears to shrink.
272. This type is characterised by increased
number of cells in the glomerulus
(hypercellular).
Usually present as a nephritic syndrome and
usually progress to end-stage renal failure
(ESRF) over weeks to years
Types
IgA nephropathy (Berger's disease)
Henoch-Schönlein purpura
Membranoproliferative/mesangiocapillary GN
Rapidly progressive glomerulonephritis
273. IgA nephropathy usually presents as macroscopic
haematuria (visibly bloody urine). It occasionally
presents as a nephrotic syndrome.
It often affects young males within days (24-
48hrs) after an upper respiratory tract or
gastrointestinal infection.
It shows increased number of mesangial cells
with increased matrix (the 'cement' which holds
everything together).
Immuno-staining is positive for IgA deposits
within the matrix.
Prognosis is variable, 20% progress to ESRF.
ACE inhibitors are the mainstay of treatment
274. HSP is a systemic variant of IgA
nephropathy which causes a small-
vessel vasculitis and associated
glomerulonephritis.
275. It can occur after essentially any infection,
specially with Streptococcus pyogenes.
Streptococcal titers in the blood (antistreptolysin
O titers) may support the diagnosis.
It shows diffuse hypercellularity due to
proliferation of endothelial and mesangial cells,
as well as an influx of neutrophils and monocytes.
The Bowman space is compressed, in some
cases to the extent that this produces a crescent
formation characteristic of crescentic
glomerulonephritis.
Treatment is supportive, and the disease
generally resolves in 2-4 weeks.
276. This is primary, or secondary to SLE,
viral hepatitis, hypocomplementemia.
One sees 'hypercellular and
hyperlobular' glomeruli due to
proliferation of both cells and the matrix
within the mesangium.
Presents usually with as a nephrotic
syndrome, with inevitable progression to
ESRF.
277. Crescentic glomerulonephritis induced by
infective endocarditis
It is demonstrated circumferential and cellular
crescent formation with interstitial nephritis.
It has a poor prognosis, with rapid
progression to kidney failure over weeks.
Steroid therapy is sometimes used
Any of the above types of GN can be rapidly
progressive.
278. Additionally two further causes present
as solely RPGN.
1. Goodpasture's syndrome, an
autoimmune disease whereby antibodies
are directed against basal membrane
antigens found in the kidney and lungs. As
well as kidney failure, patient have
hemoptysis (cough up blood).
High dose immunosuppresion is required (IV
Methylprednisolone) and cyclophosphamide,
plus plasmapheresis.
279. 1. Wegener's granulomatosis and polyarteritis.
There is a lack of immune deposits on staining,
but blood tests are positive for ANCA.
The majority of glomeruli present "crescents".
Formation of crescents is initiated by passage
of fibrin into the Bowman space as a result of
increased permeability of glomerular basement
membrane.
Fibrin stimulates the proliferation of parietal
cells of Bowman capsule, and an influx of
monocytes.
Rapid growing and fibrosis of crescents
compresses the capillary loops and decreases
the Bowman space which leads to renal failure
within weeks or months.
280. Hereditary: result from a gene on the X chromosome
passed on from carrier mothers who have no features,
or minimal features of the problem,
Idiopathic
Infections
• Post streptococcal GN: Beta hemolytic
streptococcal infection, URTI. Called as acute
poststreptococcal glomerulonephritis, or APSGN.
• Bacterial endocarditis
• Viral infections e.g. hep. B,C AIDS
• Fungal and parasitic
282. dark brown-colored urine
(from blood and protein)
sore throat
diminished urine output
fatigue
lethargy
increased breathing effort
headache
high blood pressure
seizures (may occur as a
result of high blood
pressure)
rash, especially
over the buttocks
and legs
weight loss
joint pain
pale skin color
fluid accumulation
in the tissues
(edema) in m’ing
283. S/S of Kidney failure
• Lack of appetite
• Nausea
• Vomiting
• Fatigue
• Difficulty in sleeping
• Dry /itchy skin
• Muscle cramps at night
284. Any1or 2 degree infection
Immune response activates
Antibodies formed in response to antigen
Antigen-antibody complex formed
Deposition of immune complex in
glomeruli
285. Soluble circulating complexes lodge in filtration
barrier
Complex bind and activate complement which
enhances migration of WBCs to site
WBCs release proteolytic enzyme from
lysosomes
Damages the glomerular cells
Results in filtration barrier being damaged
286. If Damage Is
Great
Dec. Functional
Surface area
Dec. GFR
Azotemia
Majority glomeruli
affected
Hyalinization
Dilated tubules with
hyalin casts
ESRD
Permeability es
Allows more proteins
to leave the cappilary
lumen and RBC
Proteinuria &
hematuria
Foamy cola coloured
urine
291. Strep or other bacterial infection: antibiotic.
Lupus or vasculitis. : corticosteroids and immune-
suppressing drugs.
IgA nephropathy: Fish oil supplements
Goodpasture's syndrome. Plasmapheresis
Plasmapheresis is a mechanical process that
removes antibodies from your blood by taking
the plasma out of your blood and replacing it
with fluid or donated plasma.
292. Acute kidney failure. Loss of function in the
filtering part of the nephron may cause waste
products to accumulate rapidly.
Chronic kidney failure. the kidneys gradually lose
function. usually requires dialysis or a kidney
transplant
High blood pressure. Damage to your kidneys and
the resultant buildup of wastes in the bloodstream can
raise your blood pressure.
Nephrotic syndrome. may accompany
glomerulonephritis and other conditions that affect
the filtering ability of the glomeruli.
UTI
Fluid overload
301. The nephrotic syndrome is characterized by
heavy proteinuria (more than 3.5g protein)
and is usually associated with
hypoalbuminemia ,hyperlipidemia and
edema.
302. The increased
glomerular permeability
found in nephrotic
syndrome is responsible
for massive excretion of
proteins in urine.
This results in decreased
serum protein and
subsequent edema
formation.
303. The normal glomerular capillary wall
keeps blood cells and most proteins in
the blood.
In patients with proteinuria, protein
leaks across the wall into the urine.
304. The barriers in the capillary wall that
keep protein out of the urine are
1. the endothelial cell lining the capillary
lumen
2. the basement membrane
3. epithelial cells (podocyte) normally
has little “feet” (pods) that sit on the
basement membrane and are
connected by a thin membrane.
podocytes appear to be the most
important barrier that prevents protein
from leaking into the urine
311. Becoz of immunologic, inflammatory or metabolic
abnormality(DM) ,HTN, GN
Increased glomerular basement membrane permability
or glomerulus get damaged
Low mol wt proteins such as albumin and alpha-globulin
are excreted in excess amt
Albumin synthesis and production imbalances
Hypoalbuminemia
312. Decreased plasma oncotic
pressure
Fluid shifts to interstitial space
from intravascular
Compartment
Decreased intravascular vol
Decreased renal blood flow
Decreased GFR
Stimulation of production of
aldosterone and ADH
Excessive sodium and water
retention leading to edema
Urinary loss of
inhibitors of clotting
(antithrombin3)
Thrombosis Stimulates hepatic
lipoprotein
synthesis
Hyperlipidemia
Fat bodies appear
in urine
313. Proteinuria(>3.5g/day),
hypoalbuminemia,
hyperlipidemia
edema.
A few other characteristics are:
1. Excess fluid in the body.
• Puffiness around the eyes,
(morning)
• Edema over the legs which is
pitting
• pleural effusion.
• pulmonary edema.
• ascites.
314. 2. Hypertension (rarely)
3. foamy urine, due to a lowering of the surface
tension by the severe proteinuria.
4. hematuria or oliguria are uncommon, and
are seen commonly in nephritic syndrome.
5. rash associated with Systemic Lupus
Erythematosus,
6. neuropathy associated with diabetes.
315. Urine sample shows proteinuria (>3.5 per
1.73 m2 per 24 hour).
Hypoalbuminemia: albumin level ≤2.5g/dL
(normal=3.5-5g/dL).
hypercholesterolemia, elevated LDL, usually
with concomitantly elevated VLDL
Electrolytes, urea and creatinine (EUCs)
Biopsy of kidney
Auto-immune markers (ANA, ASOT, C3,
cryoglobulins, serum electrophoresis)
316. Monitoring and maintaining euvolemia
monitoring urine output, BP regularly
fluid restrict to 1L
diuretics (IV furosemide)
Monitoring kidney function
do EUCs daily and calculating GFR
Prevent and treat any complications
Albumin infusions are generally not used
because their effect lasts only transiently.
Prophylactic anticoagulation may be
appropriate in some circumstances.
317. Immunosupression (corticosteroids, cyclosporin).
Standard ISKDC regime for first episode:
prednisolone -60 mg/m2/day in 3 divided doses
for 4 weeks followed by 40 mg/m2/day in a single
dose on every alternate day for 4 weeks.
Frequent relapses treated by: cyclophosphamide
or nitrogen mustard or cyclosporin or levamisole.
blood glucose control if diabetic.
Blood pressure control. ACE inhibitors (they have
been shown to decrease protein loss)
318. Venous thrombosis: due to leak of anti-
thrombin 3, which helps prevent thrombosis.
This often occurs in the renal veins. Treatment
is with oral anticoagulants (not heparin as
heparin acts via anti-thrombin 3 which is lost in
the proteinuria so it will be ineffective.)
Infection: due to leakage of immunoglobulins,
encapsulated bacteria such as Haemophilus
influenzae and Streptococcus pneumonia can
cause infection.
Acute renal failure is due to hypovolemia.
Pulmonary edema
319. Growth retardation:It occurs in cases
of relapses or resistance to therapy.
Causes of growth retardation are protein
deficiency from the loss of protein in
urine, anorexia (reduced protein intake),
and steroid therapy (catabolism).
Vitamin D deficiency
Thyroxin is reduced due to decreased
thyroid binding globulin.
Microcytic hypochromic anaemia
320. Nursing Assessment
Assess edema
Check daily wt
Accurate I/O
Measure abdominal girth/ extremity size
Assess skin condition
Assess for effectiveness of treatment
Avoid trauma
Effectiveness of diuretic therapy
321. Clinical Problem Nursing Diagnosis Nursing
Intervention
Retention of
sodium and fluid
Edema
Altered fluid and
electrolyte balance
R/T retention of
sodium and fluid
Impaired skin
integrity R/T edema
-Check daily
weight -
Measure abdominal
girth
-Maintain I/O chart
-Low sodium diet
-Monitor
electrolytes
-Assess for the skin
integrity
-Keep pt dry
322. Clinical Problem Nursing Diagnosis Nursing
Intervention
-Turn the pt
frequently
-Maintain hygiene
-Relieve pressure
from pressure
points
-Use air or water
mattresses
-Provide scrotal
support in men
323. Clinical
Problem
Nursing Diagnosis Nursing
Intervention
Protein loss Altered nutritional
pattern R/T protein
loss
-Assess for S/S of
infection
-Serve small
frequent feedings
-Protein intake 1.0
to 1.5 per kg of
body wt
-Serve food in an
attractive manner
-Ask for the likes
and dislikes of pt
324. Clinical Problem Nursing Diagnosis Nursing
Intervention
Low immunity Potential for
infection R/T
intake of
immunosuppressiv
e drugs
-Maintain hygiene
-Use aseptic
technique
-Avoid exposure
to persons with
known infections
-Avoid invasive
procedures or
maintain strict
asepsis
326. Clinical Problem Nursing Diagnosis Nursing
Intervention
Edema Altered body
image R/T
puffiness of face
and edema of legs
-Restrict fluids
and sodium
-provide
knowledge
regarding the
causes for edema
-Ventilate his fears
-Remove the
mirrors from the
room to avoid him
to look his face
327.
328. The normal function of the urinary bladder is
to store and expel urine in a coordinated,
controlled fashion. This coordinated activity
is regulated by the central and peripheral
nervous systems. Neurogenic bladder is a
term applied to a malfunctioning urinary
bladder due to neurologic dysfunction or
insult emanating from internal or external
trauma, disease, or injury.
329. Neurogenic bladder refers to dysfunction
of the urinary bladder due to disease of the
central nervous system or peripheral
nerves involved in the control of
micturition.
331. Herniated disc
Injuries that crush pelvis
Lumbar laminectomy
Radical hysterectomy
Abdominoperineal resection
Peripheral nerve injury
Diabetes mellitus
AIDS
poliomyelitis
Guillain-Barré syndrome
severe herpes in the genitoanal area
pernicious anemia
neurosyphilis (tabes dorsalis)
332. urinary tract infection
kidney stones - these may be difficult to determine
because you may not be able to feel pain associated
with kidney stones if you have spinal cord
abnormalities. Symptoms of kidney stones include:
chills
shivering
fever
urinary incontinence
small urine volume during voiding
urinary frequency and urgency
dribbling urine
loss of sensation of bladder fullness
333. Lab studies
Urinalysis and urine culture
Urine cytology
Chem 7 profile: Blood urea nitrogen (BUN) and
creatinine
Other tests
Voiding diary: A voiding diary is a daily record of the
patient's bladder activity
Pad test :This is an objective test that documents the
urine loss. Intravesical methylene blue test or oral
Pyridium or Urised may be used. Methylene blue and
Urised turns the urine color blue; Pyridium turns the
urine color orange.
Diagnostic procedures
Postvoid residual urine
334. Uroflow rate :Uroflow rate is volume of urine
voided per unit of time.
Filling cystometrogram
filling cystometrogram
Voiding cystometrogram (pressure-flow study)
Cystogram
Electromyography
Cystoscopy
Videourodynamics
336. Stress incontinence may be treated with
surgical and nonsurgical means.
Urge incontinence may be treated with
behavioral modification or with bladder-
relaxing agents.
Mixed incontinence may require
medications as well as surgery.
Overflow incontinence may be treated with
some type of catheter regimen.
Functional incontinence may be resolved
by treating the underlying cause (eg,
urinary tract infection, constipation) or by
simply changing a few medications.
337. Absorbent products :Absorbent products
are pads or garments designed to absorb
urine to protect the skin and clothing.
Urethral occlusive devices :Urethral
occlusive devices are artificial devices that
may be inserted into the urethra or placed
over the urethral meatus to prevent urinary
leakage.
Catheters
Indwelling urethral catheters
suprapubic tubes
self-intermittent catheterization.
338. Surgical care for stress incontinence involves
procedures that increase urethral outlet
resistance. Operations that increase urethral
resistance include :
bladder neck suspension
periurethral bulking therapy
sling procedures
artificial urinary sphincter
Surgical care for urge incontinence involves
procedures that improve bladder compliance or
bladder capacity.
sacral neuromodulation
botulinum toxin injections,
detrusor myomectomy
bladder augmentation
339. Avoidance of dietary stimulants
avoiding spicy foods like curry, chili
pepper, cayenne pepper, and dry mustard.
Avoiding citrus fruits like grapefruits and
oranges.
Avoiding chocolate-containing sweets.
Chocolate snacks
Avoiding treats contain caffeine
341. Pelvic floor exercise
Vaginal weights : Vaginal weights are
tamponlike special help aids used to
enhance pelvic floor muscle exercises..
Biofeedback :Biofeedback therapy is a
form of pelvic floor muscle rehabilitation
using an electronic device for individuals
having difficulty identifying levator ani
muscles. These devices allow the patient
to receive immediate visual feedback on
the activity of the pelvic floor muscles.
342. Electrical stimulation :Electrical stimulation
is a more sophisticated form of biofeedback
used for pelvic floor muscle rehabilitation.
This treatment involves stimulation of levator
ani muscles using painless electric shocks.
Bladder training: Bladder training generally
consists of self-education, scheduled voiding
with conscious delay of voiding, and positive
reinforcement.
343. Medications
Sympathomimetic drugs
estrogen
tricyclic agents
The 3 main categories of drugs used to
treat urge incontinence include :
anticholinergic drugs
antispasmodics
tricyclic antidepressant agents
When a single drug treatment does not
work, combination therapy, such as
oxybutynin (Ditropan) and imipramine
(Tofranil) may be used.
.
347. unique to suprapubic catheter
skin infection
hematoma
bowel injury
problems with catheter reinsertion
Untreated urinary tract infections may lead
to urosepsis and death.
348. Excellent
Depends on the underlying condition
that has precipitated urinary
incontinence
Urinary incontinence itself is easily
treated and prevented by properly
trained health care individuals.
349.
350. The urinary bladder occupies the deep pelvic
cavity and is well protected.
Because the bladder is located within the
bony structures of the pelvis, it is protected
from most external forces. This is the reason
it is rarely traumatized.
However it can suffer traumas which can
cause extraperitoneal and intraperitoneal
ruptures
351. It is the injury to the urinary bladder caused by
either blunt or penetrating accidents.
The probability of bladder injury varies
according to the degree of bladder distention;
therefore, a full bladder is more likely to
become injured than an empty one.
353. Penetrating and blunt trauma (main causes of
bladder injury) during accidents.
Iatrogenic causes include surgical
misadventures from gynecologic, urologic, and
orthopedic operations near the urinary bladder.
Spontaneous or idiopathic bladder injuries
without an obvious underlying pathology
constitute the remainder.
354. Other causes include:
Surgeries of the pelvis or groin (including
hernia repair and abdominal hysterectomy)
Tears, cuts, bruises, and other injuries to the
urethra (most common in men)
Straddle injuries (direct force accidents that
injure the scrotum area between a man's legs)
Deceleration injury (for example, a motor
vehicle accident that occurs with a full bladder
while wearing seatbelt)
355.
356. ◦ The most common mechanisms of blunt trauma
are road traffic accidents (87%), falls (7%), and
assaults (6%).
Deceleration injuries usually produce both
bladder trauma (perforation) and pelvic fractures.
◦ Approximately 10% of patients with pelvic fractures also
have significant bladder injuries.
357. ◦ The likelihood of the bladder to sustain injury is
related to its degree of distention at the time of
trauma.
◦ Injury may occur if there is a blow to the pelvis
that is severe enough to break the bones and
cause bone fragments to penetrate the bladder
wall.
◦ Generally the bladder injury in these cases is
associated with other injuries as well, the
commonest being to the spleen and rectum.
358. The most common cause of penetrating trauma is
gunshot wounds (85%), followed by stabbings
(15%).
It is also associated with abdominal and/or pelvic
organ injuries.
Combined penetrating trauma of the rectum and
urinary bladder is rare.
The combination of penetrating trauma to both
rectum and the urinary system is associated with
high morbidity and mortality.
359. During prolonged labor or a difficult forceps
delivery, persistent pressure from the fetal head
against the mother's pubis can lead to bladder
necrosis.
• Direct laceration of the urinary bladder is reported
in 0.3% of women undergoing a Caesarean
delivery.
• Previous Caesarean deliveries, and the adhesions
that can remain subsequently, are a risk factor.
360. • Bladder injury may occur during a vaginal or
abdominal hysterectomy.
• Blind dissection in the incorrect tissue plane
between the base of the bladder and the
cervical fascia results in bladder injury.
361. Perforation of the bladder during a bladder
biopsy, cystolitholapaxy, transurethral
resection of the prostate (TURP), or
transurethral resection of a bladder tumor
(TURBT) is common.
Incidence of bladder perforation is reportedly
as high as 36% following bladder biopsy.
362. Orthopedic pins and screws can
commonly perforate the urinary bladder,
particularly during internal fixation of
pelvic fractures.
Thermal injuries to the bladder wall may
occur during the setting of cement
substances used to seat arthroplasty
prosthetics.
363. • Alcoholics and those individuals
who chronically drink large
quantities of fluids are susceptible
to this type of injury (bladder over
distension )
Person who holds urine for long
time during over distension.
364. Type I injuries are partial tears of the mucosa.
This is the most common injury pattern of
multisystem trauma patients and is associated
with blunt trauma.
Type II or intraperitoneal bladder ruptures.
This is usually the result of a direct blow to the
distended organ.
365. Type III or interstitial pattern. This is an intramural or
partial-thickness laceration of the intact serosa. CT
cystography is used to diagnose this. Intramural
contrast is shown within the bladder wall. This
condition is usually the result of blunt trauma.
Type IV bladder injury is extraperitoneal. It is the
most common bladder rupture. It is subdivided into
simple and complex injuries.
366. Extraperitoneal bladder ruptures
• Traumatic extraperitoneal ruptures are usually
associated with pelvic fractures (89%-100%). The
bladder rupture is most often due to a direct burst
injury or the shearing force of the deforming pelvic
ring.
• These ruptures are usually associated with
fractures of the anterior pubic arch, and they may
occur from a direct laceration of the bladder by the
bony fragments of the osseous pelvis.
367. • The anterolateral aspect of the bladder is
typically perforated by bony spicules.
Forceful disruption of the bony pelvis tear
the wall of the bladder.
• The degree of bladder injury is directly
related to the severity of the fracture.
• The classic cystographic finding is contrast
extravasation around the base of the bladder
confined to the perivesical space
368. • With a more complex injury, the
contrast material extends to the
thigh, penis, perineum, or into the
anterior abdominal wall.
• The bladder may assume a teardrop
shape from compression by a pelvic
hematoma.
369. Classic intraperitoneal bladder ruptures are
described as large horizontal tears in the dome
of the bladder. The dome is the least supported
area and the only portion of the adult bladder
covered by peritoneum.
The mechanism of injury is a sudden large
increase in intravesical pressure in a full
bladder.
370. When full, the bladder's muscle fibers are
widely separated and the entire bladder wall is
relatively thin, offering relatively little
resistance to perforation from sudden large
changes in intra vesical pressure.
Intraperitoneal bladder rupture occurs as the
result of a direct blow to a distended urinary
bladder.
371. This type of injury is common among
patients diagnosed with alcoholism or
those sustaining a seatbelt or steering
wheel injury.
Since urine may continue to drain into
the abdomen, intraperitoneal ruptures
may go undiagnosed from days to weeks.
372. Electrolyte abnormalities (e.g.,
hyperkalemia , hypernatremia, uremia,
acidosis) may occur as urine is reabsorbed
from the peritoneal cavity.
Such patients may appear anuric, and the
diagnosis is established when urinary
ascites are recovered during paracentesis.
373. Intraperitoneal ruptures demonstrate contrast
extravasation into the peritoneal cavity, often
outlining loops of bowel and pooling under the
diaphragm.
An intraperitoneal rupture is more common in
children because of the relative intra-
abdominal position of the bladder. The bladder
usually descends into the pelvis by age 20
years.
374. Clinical signs of bladder injury are relatively
nonspecific; however, a triad of symptoms are
often present: GROSS HEMATURIA
SUPRAPUBIC
PAIN OR
TENDERNESS
DIFFICULTY OR
INABILITY TO
VOID
375. Hematuria invariably accompanies all
bladder injuries. Gross hematuria is the
hallmark of a bladder rupture.
More than 98% of bladder ruptures are
associated with gross hematuria, and 10%
are associated with microscopic
hematuria.
376. An abdominal examination may reveal
distention, guarding, or rebound
tenderness.
Absent bowel sounds and signs of
peritoneal irritation indicate a possible
intraperitoneal bladder rupture.
A rectal examination should be performed
to exclude rectal injury.
377. Shock or hemorrhage (the symptoms include)
Increased heart rate
Pale skin
Sweating
Skin cool to touch
Drowsiness
Lethargy
Decreased alertness
Coma
378. History of trauma
Gross hematuria
Suprapubic pain
Difficulty to void
Abdominal tenderness
Foley’s catheter
CT scanning
Cystography
379. It is often the first test performed in patients
with blunt abdominal trauma.
The CT scan of the pelvis provides
information on the status of the pelvic organs
and bony pelvis .
It most sensitive test for bladder perforation
380. The European Association of Urology (EAU)
developed guidelines for the appropriate
management of genito-urinary trauma.
In suspected renal injuries the hemodynamic
situation of the patient is the benchmark for
the diagnostic and therapeutic algorithm.
381. Most extraperitoneal ruptures can be
managed safely with simple catheter
drainage (ie, urethral or Suprapubic).
Leave the catheter in for 7-10 days and
then obtain a cystogram.
All extraperitoneal bladder injuries heal
within 3 weeks
382. Intraperitoneal bladder rupture
Most require surgical exploration, as they do
not heal with catheterization alone. Urine
continues to leak into the abdominal cavity,
resulting in urinary ascites, abdominal
distention, and electrolyte disturbances.
All wounds should be explored and should be
surgically repaired.
383. Extraperitoneal extravasation
Bladders with extensive extraperitoneal
extravasation are often repaired
surgically.
Early surgical intervention in these cases
decreases the length of hospitalization
and potential complications. It also
promotes early recovery.
385. The patient should return in 7-10 days for
staple removal and wound check.
The X-ray cystogram should be done 10-14
days after surgery.
If the cystogram finding is normal, the urethral
catheter can be removed.
Advise the patient that they may return to
normal activity 4-6 weeks after surgery.
387. 1) Hypovolemia related to gross hemorrhage.
2) High risk for infection related to
extravasation of urine and open wounds.
3) Acute pain related to injury of the bladder.
4) Fluid and electrolyte imbalance related to
hemorrhage.
5) Anemia related to gross hematuria.
388.
389. Hydronephrosis is
distention and
dilation of the renal
pelvis and calyces,
usually caused by
obstruction of the
free flow of urine
from the kidney,
leading to
progressive atrophy
of the kidney
390.
391. The obstruction may be either
partial
complete
and can occur anywhere from the
urethral meatus to the calyces of the
renal pelvis.
