KEPERAWATAN SISTEM

URINARIA

Ns. Zaenal Abidin, M.Kep.,M.H

Keperawatan Medikal Bedah

UNIVERSITAS BOROBUDUR
JAKARTA
2020
 SISTEM URINARIA
• Fungsi ginjal (ren)
• Anatomi ginjal
• Proses produksi urine
– Filtrasi oleh glomerulus
– Reabsorbsi oleh tubulus
– Sekresi oleh tubulus
• Evaluasi fungsi ginjal
• Transportasi, penyimpanan, dan ekskresi urine
Fungsi ginjal:
1.Regulasi komposisi ion darah
2.Regulasi pH darah
3.Regulasi volume darah
4.Regulasi tekanan darah
5.Pemeliharaan osmolaritas darah (300
mOsm/l)
6.Produksi hormon (calcitriol &
erythropoetin)
7.Regulasi tingkat glukosa darah
8.Ekskresi sampah benda asing
 Anatomi Ginjal
• Anatomi eksternal:
– Retroperitoneal
• Renal fascia
• Adipose capsule
• Renal capsule
– Renal hilum

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http://www.netterimages.com/images/vtn/000/000/002/2122-150x150.jpg
Nephroptosis (Ginjal melayang/ mengambang)
• Orang amat kurus  kapsula adiposa & fasia renalis
berkurang  ginjal turun dari posisi normal
• Akibat: ureter tertekuk  blokade urine & sakit
• Insidensi: 1 dari 4 orang  kelemahan jaringan fibrosa
• Perempuan 10 X > Laki-laki
 Anatomi Ginjal

• Anatomi internal
– Cortex renalis
– Medulla renalis
– Pyramid renalis
– Papilla renalis
– Collumna renalis
– Ductus papillaris
– Calyx minor
– Calyx major
– Pelvis renalis
– Sinus renalis
http://images.google.co.id/imgres?imgurl=http://academic.kellogg.cc.mi.us/herbrandsonc/bio201_McKinley/f27-9a_urinary_bladder_c.jpg&imgrefurl=http://academic.kellogg.cc.mi.us/herbrandsonc/bio201_McKinley/Urinary%2520System.htm&h=490&w=800&sz=135&hl=id&s tart=3&tbnid=PjiUmIL-
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http://kidney.niddk.nih.gov/kudiseases/pubs/solitarykidney/images/nephronkidA.gif
 http://images.google.co.id/imgres?imgurl=http://academic.kellogg.cc.mi.us/herbrandsonc/bio201_McKinley/f27-
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Nephron:
1. Renal corpuscle :
a. Glomerulus
b. Bowman’s capsule
2. Renal tubule:
a. Proximal convoluted tubule
b. Loop of Henle
c. Distal convoluted tubule
Collecting duct
Papillary duct
http://www.farmakologija.com/materia/images/nephron.gif

http://coe.fgcu.edu/faculty/greenep/kidney/glomer3.jpg
 Vaskularisasi Ginjal
• Renal artery Renal vein

• Segmental arteries

• Interlobar arteries Interlobar veins

• Arcuate arteries Arcuate veins

• Interlobular arteries Interlobular veins

Peritubular venules
• Afferent arterioles
Peritubular capillaries

• Glomerular capillaries Efferent arterioles Vasa recta

http://www.geocities.com/biology_4e/cross_section_of_kidney.jpg
http://images.google.co.id/imgres?imgurl=http://academic.kellogg.cc.mi.us/herbrandsonc/bio201_McKinley/f27-
9a_urinary_bladder_c.jpg&imgrefurl=http://academic.kellogg.cc.mi.us/herbrandsonc/bio201_McKinley/Urinary%2520System.htm&h=490&w=800&sz=135&hl=id&start=3&tbnid=PjiUmIL-
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• Ginjal = 0.5% total body mass
• 20-25% cardiac output istirahat via arteri renalis
• Renal blood flow = 1200 mL/ menit
PROSES PRODUKSI URINE
1.Filtrasi oleh glomerulus
2.Reabsorbsi oleh tubulus
3.Sekresi oleh tubulus

http://www.colorado.edu/eeb/web_resources/cartoons/nephr.gif
 Filtrasi oleh Glomerulus
• Filtrat glomerular = 150 l (F)/ 180 l (M); Fraksi filtrasi (16-
20%); 99% filtrat direabsorbsi (ekskresi 1-2 l)
• Net filtration pressure (NFP)
1. Glomerular blood hydrostatic pressure (GBHP) = 55 mmHg
2. Capsular hydrostatic pressure (CHP) = 15 mmHg
3. Blood colloid osmotic pressure (BCOP) = 30 mmHg
NFP = GBHP – CHP – BCOP = 10 mmHg
• Glomerular Filtration Rate (GFR): jumlah filtrat
terbentuk di dalam corpusculi renalis per menit =
125 ml/min (M) atau 105 ml/min (F)

• Regulasi GFR
1. Autoregulasi renal
1. Mekanisme myogenik
2. Umpan balik tubuloglomerular
2. Regulasi saraf simpatis
3. Regulasi hormonal
1. Angiotensin II
2. Atrial natriuretic peptide (ANP)
1. Autoregulasi renal
1. Mekanisme myogenik:
BP  RBF  GFR  regangan arteriola afferent 
kontraksi otot arteriola afferent  lumen menyempit 
GFR ke tingkat semula

2. Umpan balik tubuloglomerular:

BP  GFR  cairan lewat cepat di tubulus 
rebasorbsi Na, Cl, air di PCT & loop of Henle 
deteksi oleh macula densa  inhibisi sekresi NO 
arteriola afferen konstriksi  RBF  GFR ke normal
http://images.google.co.id/imgres?imgurl=http://academic.kellogg.cc.mi.us/herbrandsonc/bio201_McKinley/f27-
9a_urinary_bladder_c.jpg&imgrefurl=http://academic.kellogg.cc.mi.us/herbrandsonc/bio201_McKinley/Urinary%2520System.htm&h=490&w=800&sz=135&hl=id&start=3&tbnid=PjiU
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2. Regulasi saraf simpatis  norepinephrine

1. istirahat: stimulasi rendah  arteriola a & e dilatasi  autoregulasi

renal & GFR tetap

2. stimulasi moderat: arteriola a & e konstriksi  restriksi aliran darah

masuk & keluar glomerulus  GFR sedikit

3. stimulasi kuat: vasokonstriksi arteriola a > e  RBF  GFR  urine

 aliran darah ke jaringan lain
Prinsip-prinsip Reabsorbsi & Sekresi Tubulus
• Reabsorbsi: 99% air dikembalikan ke darah
• Tubulus proximalis berperan besar dalam reabsorbsi
• Reabsorbsi: Na+, K+, Ca2+, Cl- , HCO3- , HPO42-
• Protein & peptida  reabsorbsi pinositosis
• Tubulus distalis  “fine tuning” reabsorbsi
• Sekresi: H+, K+, NH4+, kreatinin, obat-obatan (penisilin)
– Sekresi H+  kontrol pH darah
– Sekresi substansi sampah
• Rute reabsorbsi:
– Paraseluler & Transeluler
• Mekanisme transport:
– Transport aktif primer (hidrolisis ATP)
– Transport aktif sekunder (symporters & antiporters)
– Transport maksimum (mg/min)  glukosa darah > 200 mg/ml
• 90% air direabsorpsi bersama Na+, Cl-, dan glukosa  reabsorpsi
air wajib (obligatory water reabsorption)

• 10% air (10 – 20 L/ hari) direabsorpsi (tubulus kolektivus, oleh

ADH)  reabsorpsi air fakultatif (facultative water reabsorption)
Substansi Terfiltrasi, Direabsorpsi, & Diekskresikan ke Dalam Urine

Susbtansi Terfiltrasi* Reabsorpsi Urine

Air 180 L 178 – 179 L 1–2L
Protein 2,0 g 1,9 g 0.1 g
Na+ 579 g 575 g 4g
Cl- 640 g 633,7 g 6,3 g
HCO3- 275 g 274,97 g 0,03 g
Glukosa 162 g 162 g 0g
Urea 54 g 24 g 30 g**
K+ 29,6 g 29,6 g 2,0 g***
Asam urat 8,5 g 7,7 g 0,8 g
Kreatinin 1,6 g 0g 1,6 g
* Dengan asumsi GFR = 180 l/ hari; **Selain difiltrasi & direabsorpsi, urea
disekresi; ***K+ difiltrasi & semua direabsorpsi oleh tubulus kontortus & ansa Henle,
& disekresi oleh sel principal duktus kolektivus
Rebasorbsi & Sekresi di Tubulus Proximalis

http://people.eku.edu/ritchisong/554images/proximal_tubule.jpg

• Reabsorbsi ion (terutama Na+ dan air terbesar; 65%)

• Reabsorbsi dng sistem Na+ symport: glukosa & asam amino
(100%), asam laktat, ion-ion fosfat (HPO42-) dan sulfat (SO42-)
• Sistem Na+ /H+ antiport: Na+ dan HCO3- (80-90%)
• Osmosis air (tub. prox. & descending limb of Henle -> permeable)
• Difusi pasif: Cl- (50%), K+ (65%), Ca2+, Mg2+, HPO42+
• Hepatosit: Ammonia (NH3)  urea  filtrasi & sekresi
• Deaminasi asam amino  ammonia
Reabsorbsi di Loop of Henle
• Akhir tubulus proximalis: osmolaritas = darah
• Loop of Henle:
– Descending limb  reabsorbsi 15% air
– Thick ascending limb  impermeable thd. air
– Reabsorbsi HCO3- (10-20%)
• Sistem Na+ -K+ -2Cl- symport:
– Reabsorbsi Na+ & Cl- (35%)
– K+ kembali ke tubulus
• Reabsorbsi kation: Na+, K+,Ca2+ (20-30%), Mg2+
• Akhir loop of Henle: osmolaritas
http://www.mscd.edu/~biology/2320course/2320images/nephron.jpg
Reabsorbsi di Tubulus Distalis
• Sistem Na+ -Cl- symport
• Hormon parathyroid  reabsorbsi Ca2+
• Reabsorbsi air 10-15%
• Akhir tubulus distalis: 90-95% ion & air terserap

http://www.varimed.hu/hypertension/pha/img/pha_577.gif
Reabsorbsi & Sekresi di Ductus Collectivus
Principal cells: reabsorbsi Na+ & sekresi K+
• Intercalated cells: reabsorbsi K+ & HCO3- ;
sekresi H+

http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/N/nephron.gif
Regulasi Reabsorbsi & Sekresi oleh Hormon
• Sistem Renin – Angiotensin – Aldosteron
• Vol darah  sel juxtaglomerular

renin angiotensin
converting enzyme

angiotensinogen  angiotensin I  angiotensin II

• Angiotensin ll:
1. Vasokonstriksi arteriola afferent  GFR
2. Reabsorbsi Na+, Cl- , dan air di tubulus proximalis
3. Stimulasi kortex adrenal  aldosteron  reabsorbsi Na+, Cl- dan
sekresi K+ di ductus collectivus  reabsorbsi air
• Hormon Antidiuretik (ADH)/ Vasopressin
• Reabsorbsi air di bagian akhir tubulus distalis &
ductus collectivus (urine = 400 – 500 mL)
• Osmolaritas plasma  osmoreseptor
hipothalamus  hipophysis  ADH  tubulus
distalis & ductus collectivus

• Atrial Natriuretic Peptide (ANP)

• Volume darah  ANP dari jantung
1. Inhibisi reabsorbsi Na & air di tubulus
proximal & ductus collectivus
2. Inhibisi sekresi aldosteron & ADH
Karakteristik Urine Normal
• Volume: 1 – 2 liter per hari
• Warna: Kuning atau kuning sawo/ kuning gading (amber),
karena urokrom (hasil pemecahan pigmen empedu) dan
urobilin (hasil pemecahan hemoglobin). Urin pekat berwarna
gelap. Diet (misal: bit merah), obat, penyakit, berpengaruh pada
warna. Batu ginjal  darah
• Turbiditas: transparan (urine baru); berkabut (dibiarkan)
• Bau: aromatik ringan (baru)  amonia (dibiarkan);
metilmerkaptan (pada orang tertentu yang makan asparagus );
bau buah (badan keton pada diabetes mellitus)
• pH: antara 4,6 – 8,0 (rata-rata 6,0). Diet tinggi protein 
asam; diet tinggi sayuran  basa
• Berat jenis: antara 1,001 – 1,035. Konsentrasi zat terlarut
meningkat  BJ meningkat
Diuresis
• Memperlambat reabsorbsi air
• Terapi hipertensi
• Diuretik alami: kopi, teh, soda (inhibisi
reabsorbsi Na+), alkohol (inhibisi ADH)
• Mekanisme kerja kebanyakan diuretik: inhibisi
reabsorbsi Na+
• Furosemide (Lasix)  inhibisi Na+ K+ 2 Cl-
symporters di thick ascending limb of the loop of
Henle
• Chlorthiazide (Diuril)  tubulus distalis (inhibisi
Na+ Cl- symporters)
Evaluasi Fungsi Ginjal
• Urinalisis
• Tes darah
– Blood Urea Nitrogen (BUN)
• Katabolisme asam amino  urea  nitrogen
• GFR  BUN
– Kreatinin plasma
• Katabolisme fosfat kreatinin dari otot skelet
• Fungsi ginjal  Kreatinin darah
– Renal plasma clearance: volume darah yang
dibersihkan dari substansi tertentu per unit per waktu
(mL/ menit)
– Renal plasma clearance substansi C = U X V
P
 Transportasi, Penyimpanan, dan Eliminasi
Urine
• Urine duktus kolektivus =
urine vesica urinaria
• Ureter (peristaltik)
• Vesica Urinaria
• Vesicoureteral reflux
• Ureterorenal reflex
(konstriksi a. afferen)
• Refleks micturitio
• Urethra
• Inkontinensia urine
http://hcd2.bupa.co.uk/images/factsheets/kidney_stones.gif
 http://academic.kellogg.cc.mi.us/herbrandsonc/bio201_McKinley/f27-9a_urinary_bladder_c.jpg
Inervasi:
1. Parasimpatis (S2 – S3  nervus pelvicus  plexus sacralis); sensoris &
motoris
2. Simpatis (L2  nervus hypogastricus): pembuluh darah
3. Somatis (nervus pudendus  m. sphincter externus)
http://images.google.co.id/imgres?imgurl=http://clem.mscd.edu/~raoa/bio2320/uriphys/img038.jpg&imgrefurl=http://clem.mscd.edu /~raoa/bio2320/uriphys/sld038.htm&h=539&w=719&sz=43&hl=id&start=1&tbnid=RIxPxSlvLPYN0M:&tbnh=105&tbnw=140&prev=/images%3Fq%3Dmic turition%2Breflex%26svnum%3D10%26hl%3Did%26lr%3D%26sa%3DG
Pengisian Vesica Urinaria

1. Vesica Urinaria kosong  Tekanan = 0 cm

air

2. Urine 30 – 50 ml  Tekanan tonik naik 5 –

10 cm air

3. Urine 200 – 300 ml  Tekanan naik sedikit

(micturition reflex)

4. Urine 300 – 400 ml  Tekanan naik cepat

• Tekanan tonik meningkat

• Kontraksi mikturisio: reseptor sensoris regang 

stretch reflex  nervus pelvicus  kontraksi m.
detrusor (bbrp detik – 1 menit; semakin penuh
semakin sering)

• “Self regenerative” micturition reflex

• Urine tidak dikeluarkan  inhibisi bbrp menit – 1

jam

• Refleks mikturisio meningkat  refleks inhibisi via

n. pudendus  m. sphincter externus
Fasilitasi & Inhibisi Mikturisio oleh Otak

1. Pusat-pusat fasilitasi & inhibisi di batang otak

terutama pons
2. Pusat-pusat di korteks serebri, terutama inhibisi
tapi dapat menjadi eksitatoris

Pengaturan miksi oleh otak/ pusat-pusat atas:

1. Inhibisi parsial
2. Mencegah mikturisio via kontraksi tonik m.
sphincter externus
3. Fasilitasi pusat mikturisio sakral  refleks
mikturisio & inhibisi m. sphincter externus

Urinasi sadar  kontraksi abdomen

Abnormalitas mikturisio
• Destruksi serabut saraf sensoris  hilang
kontrol  overflow incontinence (tabes dorsalis
pada syphilis  radiks dorsalis)

• Kerusakan spinal di atas regio sacral

• “spinal shock” kemudian refleks kembali

• Kerusakan parsial medula spinalis/ batang otak

• Sinyal inhibitoris hilang
• Impuls fasilitasi tak terkontrol  urinasi
sering, tak terkontrol
Pembentukan Urine Encer & Pekat
– Total volume cairan tubuh konstan

– Homeostasis: Ginjal memproduksi urine encer/

pekat

– ADH mengontrol kepekatan urine

Pembentukan Urine Encer

1. Osmolaritas cairan interstisiil  osmolaritas

cairan tubuler
2. Symporters Na+, K+, Cl- pada thick ascending
limb dari loop of Henle
3. Thick ascending limb tak permeable terhadap air
 150 mOsm/l di akhir loop of Henle
4. Tubulus kontortus distalis tak terlalu permeable
terhadap air & tak diregulasi oleh ADH
5. Kadar ADH rendah, duktus kolektivus tak
permeable terhadap air  65 – 70 mOsm/l
• Pembentukan Urine Pekat

• Asupan air sedikit/ kehilangan air banyak

• ADH  urine pekat (4x), 1200 mOsm/l

• Gradien osmotik cairan interstisial (Na+, Cl-,

urea)

1. Perbedaan permeabilitas dan reabsorbsi air

& zat terlarut di loop of Henle panjang
(nephron juxtaglomerular) & duktus
kolektivus

2. Countercurrent flow
• Proses Produksi Urine Pekat
1. Symporters di thick ascending limb (Na+, K+, Cl-) 
gradien osmotik di medula renalis. Air tak direabsorbsi

2. Duktus kolektivus menyerap air (karena ADH)

3. Duktus kolektivus di medula bagian dalam menyerap

urea (karena difusi & permeable terhadap urea) 
akumulasi di jaringan interstisial

4. Difusi urea ke descending & thin ascending limb of

Henle

5. Urea tetap di lumen thick ascending limb, tubulus

distalis, duktus kolektivus kortikal (karena tak
permeable terhadap urea  siklus 2 – 4 berulang (daur
ulang urea)
Countercurrent Mechanism
• Osmolaritas cairan interstisial meningkat dari 300
mOsm/l (korteks renalis)  1200 mOsm/l (medula
renalis)

• Arah aliran descending limb >< ascending limb of

Henle

• Descending limb: Air keluar via osmosis; tak

permeable terhadap zat terlarut kecuali urea 
osmolaritas tubular (1200 mOsm/l)

• Ascending limb: Na+, Cl- symporters; tak

permeable terhadap air; osmolaritas tubular (100
mOsm/ l)
Vasa recta
• Osmolaritas awal masuk vasa recta = 300 mOsm/l

• Osmolaritas mengikuti loop of Henle

• Descending limb: Na+, Cl- masuk (cairan interstisial

 vasa recta)

• Ascending limb: Na+, Cl-, urea, keluar (vasa recta

 cairan interstisial); air masuk (cairan interstisial
 vasa recta)

• Osmolaritas akhir vasa recta = 320 mOsm/l

PENGKAJIAN KEPERAWATAN
SISTEM UROLOGI
 History of presenting complaint
Use the mnemonics SQITARS (Site, Quality,
Intensity, Timing, Aggravating factors,
Relieving factors, and associated
Symptoms)
OR
SOCRATES (Site, Onset, Character,
Radiation, Associated symptoms, Timing,
Exacerbating and alleviating factors,
Severity)
 Past medical history
• Find out any past or current medical illnesses,
operations or trauma. Past history of any renal
or urological disease is obviously important.
Diabetes and hypertension are risk factors for
CKD. Systemic diseases such as vasculitis can
cause glomerulonephritis. CKD is related to a
higher risk of cardiovascular disease. A recent
streptococcal throat infection can trigger post-
streptococcal glomerulonephritis.
Drug history
 Family history
• Polycystic kidney disease, Alport’s syndrome
and Fabry’s syndrome are inherited renal
diseases. Many other diseases will have some
genetic component. A family history of CKD
stage 5 increases the risk of an individual having
CKD. Some families have a tendency for IgA
nephropathy. Also ask about family history of
diabetes and hypertension. Ethnicity is important
in the incidence of some diseases, e.g. SLE and
diabetic nephropathy in South Asian
populations.
 Social history
• Occupation. Has the patient been exposed to any
toxins? Workers in rubber and dye factories can be
exposed to aromatic amines that can cause bladder
cancer
• Smoking is a risk factor for bladder cancer and renal
vascular disease
• Alcohol can compromise kidney function
• Dietary habits can be relevant in urolithiasis (calcium,
oxalate and fluid intake) and CKD (protein, fluid, sodium,
phosphate, iron intake)
• Sexual history may be relevant if there is a possibility of
STI
Hands
 Arms
• Look in the arms for an arteriovenous
fistula, used for dialysis access.
• If you find a fistula:
1. Palpate it to check it has a thrill
2. Auscultate over it to check it has a good
bruit.
Bruising can occur in uraemia as can
scratch marks associated with pruritus.
Face
 Chest
• Respiratory system
• Cardiovascular system
Abdomen
PEMERIKSAAN PENUNJANG
 TUGAS
1. Pemeliharaan drainase urinarius yang adekuat
2. Kateterisasi
3. Drainase kandung kemih suprapubik
4. Hemodialisa
5. Dialysis peritoneal
6. Pertimbangan preoperatif bedah ginjal
7. Permasalahan perioperatif bedah ginjal
8. Penatalaksanaan pascaoperatif bedah ginjal
9. Sistitis
10.Uretritis
11.Pielonefritis
12.Glomerulonefritis akut dan kronik
13.Sindrom nefrotik
14.Gagal ginjal akut dan kronik
15.Urolithiasis
 URAIAN TUGAS
BUAT PPT DENGAN ISI
1. KONSEP DASAR KASUS (Pengertian, etiologi,
manifestasi, patofisiologi, Pathway (Bagan
WOC), Tata laksana, pemeriksaan penunjang,
prognosis)
2. KONSEP ASUHAN KEPERAWATAN SESUAI
KASUS ( Pengkajian , Diagnosa Kep (minim 3
diagnosa), intervensi kep, Evaluasi yang
diharapkan ) DISESUAIKAN DENGAN SDKI,
SIKI, SLKI
3. DAFTAR RUJUKAN (Mininal 10 tahun terakhir)