open university of malaysia renal nursing – nbns3504
DESCRIPTION
Open University of Malaysia Renal Nursing – NBNS3504. Dr. S. Nishan Silva (MBBS). Functions of the Urinary System. Elimination of waste products Nitrogenous wastes e.g. urea, uric acid, creatinine Toxins Drugs. Functions of the Urinary System. Regulate aspects of homeostasis - PowerPoint PPT PresentationTRANSCRIPT
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OPEN UNIVERSITY OF MALAYSIARENAL NURSING – NBNS3504
Dr. S. Nishan Silva(MBBS)
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FUNCTIONS OF THE URINARY SYSTEM
Elimination of waste productsNitrogenous wastes e.g. urea, uric acid, creatinine
ToxinsDrugs
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FUNCTIONS OF THE URINARY SYSTEM
Regulate aspects of homeostasisWater balanceElectrolytesAcid-base balance in the blood (pH)Blood pressureRed blood cell productionActivation of vitamin D
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ORGANS OF THE URINARY SYSTEM
Figure 15.1a
KidneysUretersUrinary bladderUrethra
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Transverse sections show retroperitoneal position of kidneys
Note also: liver, aorta muscles on CT
Note layers of adipose (fat), capsule, fascia
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FOR STUDYING
Parts of the kidney:1. Renal pyramid2. Efferent vessel3. Renal artery4. Renal vein5. Renal hilum6. Renal pelvis7. Ureter8. Minor calyx9. Renal capsule10. Inferior renal capsule11. Superior renal capsule12. Afferent vessel13. Nephron14. Minor calyx15. Major calyx16. Renal papilla17. Renal column
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Kidney has two regionsCortex: outer
Columns of cortex divide medulla into “pyramids”Medulla: inner
Darker, cone-shaped medullary or renal pyramids Parallel bundles of urine-collecting tubules
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LOCATION OF THE KIDNEYSAt the level of T12 to L3
Attached to ureters, renal blood vessels, and nerves at renal hilus
On top of each kidney is an adrenal gland
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REGIONS OF THE KIDNEY
Figure 15.2b
Renal cortex – outer regionRenal medulla – inside the
cortexRenal pelvis – inner
collecting tube
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KIDNEY STRUCTURES
Medullary pyramids – triangular regions of tissue in the medulla
Renal columns – extensions of cortex-like material inward
Calyces – cup-shaped structures that funnel urine towards the renal pelvis
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NEPHRONS
Main structures of the nephrons
Glomerulus Renal tubule
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GLOMERULUSA specialized
capillary bedAttached to
arterioles on both sides (maintains high pressure)
Large afferent arteriole
Narrow efferent arteriole
Figure 15.3c
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BLOOD FLOW IN THE KIDNEYS
Figure 15.2c
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GLOMERULUS
Capillaries are covered with podocytes from the renal tubule
The glomerulus sits within a glomerular capsule (the first part of the renal tubule)
Figure 15.3c
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RENAL TUBULE
Glomerular (Bowman’s) capsule
Proximal convoluted tubule
Loop of HenleDescending limbAscending limbDistal
convoluted tubule
Straight collecting tubule
Figure 15.3b
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PERITUBULAR CAPILLARIES
Arise from efferent arteriole of the glomerulus
Normal, low pressure capillaries
Attached to a venule
Cling close to the renal tubule
Reabsorb (reclaim) some substances from collecting tubes
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URINE FORMATION PROCESSES
FiltrationReabsorptionSecretion
Figure 15.4
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FILTRATIONNonselective passive processWater and solutes smaller than proteins
are forced through capillary wallsBlood cells cannot pass out to the
capillariesFiltrate is collected in the glomerular
capsule and leaves via the renal tubule
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REABSORPTION
Some reabsorption is passive, most is active
Most reabsorption occurs in the proximal convoluted tubule
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SECRETION – REABSORPTION IN REVERSE
Some materials move from the peritubular capillaries into the renal tubules
Hydrogen and potassium ionsCreatinine, ureaPenicillin, cocaine, marijuana, many food preservatives, and some pesticides
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FORMATION OF URINE
Figure 15.5
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CHARACTERISTICS OF URINE USED FOR MEDICAL DIAGNOSIS
Colored somewhat yellow due to the pigment urochrome (from the destruction of hemoglobin) and solutes
ClearSterileSlightly aromaticNormal pH of around 6Specific gravity of 1.001 to 1.035
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URETERS
Continuous with the renal pelvisEnter the posterior aspect of the bladderRun behind the peritoneumPeristalsis (they contain smooth muscle)
aids gravity in urine transport
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URINARY BLADDER
Figure 15.6
Smooth, collapsible, muscular sacTemporarily stores urine
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URINARY BLADDERTrigone – three openingsTwo from the uretersOne to the urethrea
Figure 15.6
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URINARY BLADDER WALL
Composed of three layers:Outer layer – loose connective tissue covered on the upper surface by the peritoneum
Middle layer - three layers of smooth muscle (detrusor muscle)
Inner layer - mucosa made of transitional epithelium
Walls are thick and folded in an empty bladder, can expand significantly without increasing internal pressure
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THE URETHRASmooth muscle with inner mucosa Changes from transitional through stages to stratified squamous near
end Drains urine out of the bladder and bodyMale: about 20 cm (8”) longFemale: 3-4 cm (1.5”) long Short length is why females have more urinary tract infections than
males - ascending bacteria from stool contamination
Urethra____
urethra
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Urethral sphincters Internal: involuntary sphincter of smooth muscleExternal: skeletal muscle inhibits urination voluntarily until proper time (levator anni muscle also helps voluntary constriction)
Males: urethra has three regions (see right)
1. Prostatic urethra__________2. Membranous urethra____
3. Spongy or penile urethra_____
_________trigone
female
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URETHRARelease of urine is controlled by two
sphincters Internal urethral sphincter (involuntary)External urethral sphincter (voluntary)
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URETHRA GENDER DIFFERENCES
LocationFemales – along wall of the vagina and opens to the outside at the urethral meatus between the labia minora.
Males – through the prostate and penisFunctionFemales – only carries urineMales – carries urine and is a passageway for sperm cells
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STORAGE REFLEXES
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MICTURITION REFLEXES
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Micturition AKA:
Voiding Urinating Emptying the bladder
(See book for diagramexplanation p 701)
KNOW:Micturition center of brain:
pons(but heavily influenced by
higher centers) Parasympathetic: to voidSympathetic: inhibits
micturition
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URINE
ANALYSIS
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COLLECTION OF URINE
Early morning sample-qualitative
Random sample- routine24hrs sample- quantitativeMidstream sample-UTIPost prandial sample-D.M
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Clean Catch
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Specimen Collection
Supra-pubic Needle Aspiration
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24 HOUR URINE SAMPLE
1. For quantitative estimation of proteins2. For estimation of vanillyl mandelic
acid, 5-hydroxyindole acetic acid, metanephrines
3. For detection of AFB in urine4. For detection of microalbuminuria
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URINARY VOLUMENormal = 600-1550mlPolyuria- >2000mlOliguria-<400mlAnuria-complete cessation of
urine(<200ml)Nocturia-excretion of urine by a
adult of >500ml with a specific gravity of <1.018 at night (characteristic of chronic glomerulonephritis)
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COLOR & APPEARANCE Normal= clear & pale yellow1. Colourless- dilution, diabetes
mellitus, diabetes insipidus, diuretics
2. Milky-purulent genitourinary tract infection, chyluria
3. Orange-fever, excessive sweating
4. Red-beetroot ingestion,haematuria
5. Brown/ black- alkaptunuria, melanin
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URINARY PH/ REACTION
Reaction reflects ability of kidney to maintain normal hydrogen ion concentration in plasma & ECF
Normal= 4.6-8Tested by- 1.litmus paper 2. pH paper 3. dipsticks
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ODOUR
Normal= aromatic due to the volatile fatty acids
Ammonical – bacterial actionFruity- ketonuria
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SPECIFIC GRAVITY
Depends on the concentration of various solutes in the urine.
Measured by-urinometer - refractometer - dipsticks
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URINOMETER Take 2/3 of urinometer container with
urineAllow the urinometer to float into the
urineRead the graduation at the lowest
level of urinary meniscusCorrection of temperature & albumin
is a must.Urinometer is calibrated at 15or 200cSo for every 3oc increase/decrease
add/subtract 0.001For 1gm/dl of albumin add0.001
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CHEMICAL EXAMINATION
ProteinsSugarsKetone bodiesBilirubinBile saltsUrobilinogenBlood
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MICROSCOPIC EXAMINATION
Microscopic urinalysis is done simply pouring the urine sample into a test tube and centrifuging it (spinning it down in a machine) for a few minutes. The top liquid part (the supernatant) is discarded. The solid part left in the bottom of the test tube (the urine sediment) is mixed with the remaining drop of urine in the test tube and one drop is analyzed under a microscope
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CRYSTALS IN URINE
Crystals in acidic urine Uric acid Calcium oxalate Cystine Leucine
Crystals in alkaline urine Ammonium magnesium
phosphates(triple phosphate crystals)
Calcium carbonate
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CRYSTALS
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CASTSUrinary casts are cylindrical
aggregations of particles that form in the distal nephron, dislodge, and pass into the urine. In urinalysis they indicate kidney disease. They form via precipitation of Tamm-Horsfall mucoprotein which is secreted by renal tubule cells.
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TYPES OF CASTSAcellular castsHyaline castsGranular castsWaxy castsFatty castsPigment castsCrystal casts
Cellular castsRed cell castsWhite cell castsEpithelial cell cast
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GRANULAR CASTSGranular casts can result either
from the breakdown of cellular casts or the inclusion of aggregates of plasma proteins (e.g., albumin) or immunoglobulin light chains
indicative of chronic renal disease
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Microscopic Examination Granular Cast
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Microscopic Examination WBCs Cast
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Microscopic Examination RBCs Cast -
Histology
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Chemical AnalysisUrine
DipstickGlucoseBilirubinKetonesSpecific GravityBloodpHProteinUrobilinogenNitriteLeukocyte Esterase
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BLOOD ANALYSIS
(Of creatinine)
Glomerulofiltration Rate
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ESTIMATED GFR
GFR Calculatorhttp://easycalculation.com/medical/gfr.php
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RENAL SCAN
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RENAL ARTERIOGRAM
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INTRAVENOUS PYELOGRAM
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RENAL BIOPSY
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PYELO
NEPHRITI
S
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ETIOLOGY❏ usually ascending microorganisms, most often
bacteria❏ in females with uncomplicated pyelonephritis
usually E. coli❏ causative microorganisms are usually E. coli,
Klebsiella, Proteus, Serratia, Pseudomonas, Enterococcus, and S. aureus
❏ if S. aureus is found, suspect bacteremic spread from a distant focus (e.g. septic emboli in infective endocarditis) and suspect (possible multiple intra-renal microabscesses or perinephric abscess)
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CLINICAL PRESENTATION❏ rapid onset (hours to a day)❏ lethargic and unwell, fever, tachycardia,
shaking, chills, nausea and vomiting, myalgias
❏ marked CVA or flank tenderness; possible abdominal pain on deep palpation
❏ symptoms of lower UTI may be absent (urgency, frequency, dysuria)
❏ may have symptoms of Gram negative sepsis
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INVESTIGATIONS❏ urine dipstick: +ve for leukocytes and nitrites,
possible hematuria❏ microscopy: > 5 WBC/HPF in unspun urine or >
10 WBC/HPF in spun urine, bacteria❏ Gram stain: Gram negative rods, Gram positive
cocci❏ culture: > 105 colony forming units (CFU)/mL in
clean catch midstream urine or > 102 CFU/mL in suprapubic aspirate or catheterized specimen
❏ CBC and differential: leukocytosis, high % neutrophils
❏ blood cultures: may be positive in 20% of cases, especially in S. aureus infection
❏ consider investigation of complicated pyelonephritis: if fever, pain, leukocytosis not resolving with treatment within 72 hr, if male patient, or if there is history of urinary tract abnormalities (abdo /pelvis U/S, CT for renal abscess, spiral CT for stones, cystoscopy)
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COMPLICATIONSChronicityBacteraemia or Septicaemia
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TREATMENT❏ uncomplicated pyelonephritis with mild
symptoms• 14 day course of TMP/SMX (trimethoprim-sulfamethoxazole) or fluoroquinolone or third generation cephalosporin• start with IV for several days and then switch to PO (can then be treated as outpatient)
❏ patient more than mildly symptomatic or complicated pyelonephritis in the setting of stone obstruction is an urologic emergency (placing patient at risk of kidney loss or septic shock)• start broad spectrum IV antibiotics until cultures return (imipenem or emropenem or piperacillin /tazobactam or ampicillin+gentamicin) and treat 2-3 weeks• follow-up cultures 2-4 weeks after stopping treatment
❏ if no improvement in 48-72 hr, need to continue on IV antibiotics, assess for complicated pyelonephritis or possible renal or perinephric abscess
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GLOMERULONEPHRITIS
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Electron micrograph of a normal glomerular capillary loop showing the fenestrated endothelial cell (Endo), the glomerular basement membrane (GBM), and the epithelial cells with its interdigitating foot processes (arrow). The GBM is thin and no electron dense deposits are present. Two normal platelets are seen in the capillary lumen. Courtesy of Helmut Rennke, MD.
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Capillary Space
Endothelium
Urinary Space
GBM
Podocyte
FILTRATION MEMBRANE – ELECTRON MICRO.
MD consult
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82Electron micrograph in dense deposit disease (DDD) showing dense, ribbon-like appearance
of subendothelial and intramembranous material (arrow) and narrowing of the capillary lumen due to proliferation of cells (double arrow). Courtesy of Helmut Rennke, MD.
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POSSIBLE CLINICAL MANIFESTATIONSProteinuria – asymptomaticHaematuria – asymptomatic
HypertensionNephrotic syndromeNephritic syndromeAcute renal failureRapidly progressive renal failureEnd stage renal failure
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DIAGNOSIS
Look for clues History
Haematuria Proteinuria Azotemia azote – nitrogen A – without Zoe – life “The gas does not support life” (French chemists Gayton de Morveau
(1737-1816) and Antoine Lavoisier (1743-1794) )
McCarthy ET, November 2008
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NEPHROTIC SYNDROME
Nephrotic syndrome (NS) results from increased permeability of Glomeulrar basement membrane (GBM) to plasma protein.
It is clinical and laboratory syndrome
characterized by massive proteinuria, which lead to hypoproteinemia ( hypo-albuminemia), hyperlipidemia and pitting edema.
(4-increase, 1-decrease).
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NEPHROTIC CRITERIA:-
*Massive proteinuria: qualitative proteinuria: 3+ or 4+, quantitative proteinuria : more than 40 mg/m2/hr in children (selective).
*Hypo-proteinemia : total plasma proteins < 5.5g/dl and serum albumin : < 2.5g/dl.
*Hyperlipidemia: serum cholesterol : > 5.7mmol/L
*Edema: pitting edema in different degree
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NEPHRITIC CRITERIA
-Hematuria: RBC in urine (gross hematuria)
-Hypertension: ≥130/90 mmHg in school-age children ≥120/80 mmHg in preschool-age children ≥110/70 mmHg in infant and toddler’s children
-Azotemia ( renal insufficiency ) : Increased level of serum BUN 、 Cr-Hypo-complementemia: Decreased level of serum c3
Oliguria, Oedema, Albuminurea
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CLASSIFICATION:
A-Primary Idiopathic NS (INS): majority The cause is still unclear up to now. Recent 10
years ,increasing evidence has suggested that INS may result from a primary disorder of T– cell function.
Accounting for 90% of NS in child. mainly discussed.
B-Secondary NS: NS resulted from systemic diseases, such as
anaphylactoid purpura , systemic lupus erythematosus, HBV infection.
C-Congenital NS: rare*1st 3monthe of life ,only treatment renal
transplantation
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SECONDARY NS Drug,Toxic,Allegy: mercury, snake venom, vaccine, pellicillamine,
Heroin, gold, NSAID, captopril, probenecid, volatile hydrocarbonsInfection: APSGN, HBV, HIV, shunt nephropathy, reflux nephropathy,
leprosy, syphilis, Schistosomiasis, hydatid disease
Autoimmune or collagen-vascular diseases: SLE, Hashimoto’s thyroiditis,, HSP, Vasculitis
Metabolic disease: Diabetes mellitus
Neoplasma: Hodgkin’s disease, carcinoma ( renal cell, lung, neuroblastoma, breast, and etc)
Genetic Disease: Alport syn, Sickle cell disease, Amyloidosis, Congenital nephropathy
Others: Chronic transplant rejection, congenital nephrosclerosis
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IDIOPATHIC NS (INS): PATHOLOGY:-
Minimal Change Nephropathy (MCN): <80%The glomeruli appear normal basically Under
Light microscopy, and Under Immunofluorescence
*under Electron microscopy – fusion of the foot processes of the podocytes
(2) Non—MCN : < 20%*Mesangial proliferative glomerulonephritis (MsPGN): about 10%*Focal segmental glomerulosclerosis (FSGS): 5%*Membranous Nephropathy (MN) : 2% *Membrane proliferative glomerulonephritis
(MPGN) : 1% *Others : rare,Cresent glomerulonephritis
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CLINICAL MANIFESTATION:-
IN MCNS , The male preponderance of 2:1
: 1.Main manifestations: Edema (varying degrees) is the common symptom
Local edema: edema in face , around eyes( Periorbital swelling) , in lower extremities.
Generalized edema (anasarca), edema in penis and scrotum.
2-Non-specific symptoms:
Fatigue and lethargyloss of appetite, nausea and vomiting ,abdominal pain , diarrhea
body weight increase, urine output decrease pleural effusion (respiratory distress)
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INVESTIGATIONS:-
1-Urine analysis:-A-Proteinuria : 3-4 + SELECTIVE.
b-24 urine collection for protein>40mg/m2/hr for children
c- volume: oliguria (during stage of edema formation)
d-Microscopically:-microscopic hematuria 20%, large number of hyaline
cast
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INVESTIGATIONS:-
2-Blood:A-serum protein: decrease >5.5gm/dL , Albumin levels are low ( < 2.5gm/dL).
B-Serum cholesterol and triglycerides: Cholesterol > 5.7mmol/L (220mg/dl).
C-- ESR↑ > 100mm/hr during activity phase
.3.Serum complemen: Vary with clinical type.
4.Renal function
.
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KIDNEY BIOPSY:-
Considered in: 1-Secondary N.S
2-Frequent relapsing N.S
3-Steroid resistant N.S
4- Hematuria
5-Hypertension
6- Low GFR
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COMPLICATIONS OF NS:-1-Infections:Infections is a major complication in children with
NS. It frequently trigger relapses.
Nephrotic pt are liable to infection because :A-loss of immunoglobins in urine.B-the edema fluid act as a culture medium.C-use immunosuppressive agents.
D- malnutrition
The common infection : URI, peritonitis, cellulitis and UTI may be seen.
Organisms: encapsulated (Pneumococci, H.influenzae), Gram negative (e.g E.coli
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COMPLICATION …
Vaccines in NS;-
polyvalent pneumococcal vaccine (if not previously immunized) when the child is in remission and off daily prednisone therapy.
Children with a negative varicella titer should be given varicella vaccine.
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COMPLICATION…..
2-Hypercoagulability (Thrombosis).Hypercoagulability of the blood leading to venous or
arterial thrombosis:Hypercoagulability in Nephrotic syndrome caused by:
1-Higher concentration of I,II, V,VII,VIII,X and fibrinogen
2- Lower level of anticoagulant substance: antithrombin III
3-decrease fibrinolysis.
4-Higher blood viscosity
5- Increased platelet aggregation
6- Overaggressive diuresis
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3-ARF: pre-renal and renal
4- cardiovascular disease :-Hyperlipidemia, may be a risk factor for cardiovascular disease.
5-Hypovolemic shock
6-Others: growth retardation, malnutrition, adrenal cortical insufficiency
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GENERAL THERAPY:-
Hospitalization:- for initial work-up and evaluation of treatment.
Activity: usually no restriction , except massive edema,heavy hypertension and infection.
Diet Hypertension and edema: Low salt diet (<2gNa/ day) only during period of edema or salt-free diet. Severe edema: Restricting fluid intake
Avoiding infection: very important.Diuresis: Hydrochlorothiazide (HCT) : 2mg/kg.d Antisterone : 2 ~ 4mg/kg.d Dextran : 10 ~ 15ml/kg , after 30 ~ 60m, followed by Furosemide (Lasix) at 2mg/kg .
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INDUCTION USE OF ALBUMIN:-
Albumin + Lasix (20 % salt poor)
1-Severe edema2-Ascites3-Pleural effusion4-Genital edema5-Low serum albumin
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CORTICOSTEROID—PREDNISONE THERAPY:-
Prednisone tablets at a dose of 60 mg/m2/day (maximum daily dose, 80 mg divided into 2-3 doses) for at least 4 consecutive weeks.
After complete absence of proteinuria, prednisone dose should be tapered to 40 mg/m2/day given every other day as a single morning dose.
The alternate-day dose is then slowly tapered and discontinued over the next 2-3 mo.
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TREATMENT OF RELAPSE IN NS:
Many children with nephrotic syndrome will experience at least 1 relapse (3-4+proteinuria plus edema).
daily divided-dose prednisone at the doses noted earlier (where he has the relapse) until the child enters remission (urine trace or negative for protein for 3 consecutive days).
The pred-nisone dose is then changed to alternate-day dosing and tapered over 1-2 mo.
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ACCORDING TO RESPONSE TO PREDNISONE THERAPY:
*Remission: no edema, urine is protein free for 5 consecutive days.
* Relapse: edema, or first morning urine sample contains > 2 + protein for 7 consecutive days.
*Frequent relapsing: > 2 relapses within 6 months (> 4/year).
*Steroid resistant: failure to achieve remission with prednisolone given daily for 28 days.
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ALTERNATIVE AGENT:-
When can be used:
Steroid-dependent patients, frequent relapsers, and steroid-resistant patients.
Cyclophosphamide Pulse steroids
Cyclosporin A
Tacrolimus
Microphenolate
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Diseases PSGN IgA Nephropathy MPGN RPGN
Age and Sex All ages, mean 7 years, 2:1 male
2:1 male, 15-35 yrs 6:1 male, 15-30 yrs Mean 51yrs, 2:1 male
Clinical Manifestations 90% 50% 90% 90%
Acute nephritic syndrome
Occasionally 50% Rare rare
Asymptomatic haematuria
10-20% Rare Rare 10-20%
Nephrotic syndrome 70% 30-50% Rare 25%
Hypertension 50% Rare 50% 60%
Acute renal failure Latent 1-3 weeks Follows viral infection Pul haemorrhage, iron def
none
Lab findings ASOT IgA +anti GBM membrane + ANCA
Positive streptozyme IgA in dermal caps
C3-C9 N C1 and C4
Immunogenetics HLA B12
Light microscopy Diffuse proliferation Focal proliferation Focal- diffuse crescentic Crescentic GN
Immunoflourescence Granular IgG and C3 Diffuse mesangial IgA Linear IgG and C3 No immune complexes
Electron microscopy Subepithelial humps Mesangial deposits No deposits No deposits
Prognosis 95% cure5% progress
Slow progression in 25-50 years
75% stabilise or improve if treated early
75% stabilise or improve if treated early
Treatment Supportive None established Plasman exchange, cyclosphosphamide, steroids
Pulsed steroid therpy
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