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URINARIUS
I.FUNGSI GINJAL :
1.Mengatur keseimbangan air dan ion
inorganik
2.Mengeluarkan end produc metabolisme
3.Mengeluarkan benda asing
4.Glukoneogenesis
5.Memproduksi hormon / Enzim :
-Erythopoetin
-Renin / Enzim angiotensin
- 1-25 Dihydroxi vitamin D
FIGURE 162
Basic structure of a nephron. (a)
Anatomical organization. The
macula densa is not a distinct
segment but a plaque of cells in
the ascending loop of Henle where
the loop passes between the
arterioles supplying its renal
corpuscle of origin. The outer
area of the kidney is called the
cortex and the inner the medulla.
The black arrows indicate the
direction of urine flow.
(b) Consecutive segments of the
nephron. All segments in the
screened area are parts of the
renal tubule; the terms to the
right of the brackets are commonly
used for several consecutive
segments.
FIGURE 163
(a) Anatomy of the renal corpuscle. Brown lines in the capillary loops indicate space between
adjoining podocytes. (b) Cross
section of the three corpuscular membranescapillary endothelium, basement membrane, and
epithelium (podocytes) of
Bowmans capsule. For simplicity, glomerular mesangial cells are not shown in this figure.
FIGURE 164
Section of a human kidney. For clarity, the nephron illustrated
to show nephron orientation is not to scaleits outline would
not be clearly visible without a microscope. The outer kidney,
which contains all the renal corpuscles, is the cortex, and the
inner kidney is the medulla. Note that in the medulla, the loops
of Henle and the collecting ducts run parallel to each other.
The medullary collecting ducts drain into the renal pelvis.
FIGURE 165
Anatomy of the
juxtaglomerular apparatus.
FIGURE 166
The three basic components of renal function. This figure is
to illustrate only the directions of reabsorption and secretion,
not specific sites or order of occurrence. Depending on the
particular substance, reabsorption and secretion can occur at
various sites along the tubule.
.Mekanisme
Reabsorbsi :
-Transfort aktif
-Difusi
-Pinositosis
-Osmosis
Rabsorbsi
glukosa:
@glikosa difiltrasi glomerulus-Reabsobsi Tub proks---Trans aktif
@Transfort maksimum 375 mgr/menit
@Biasanya terjadi bersamaan dengan Na
REABSORBSI Na:
@65 % reabs Na di Tub proks/25 % di
Henle
REABSORBSI KLORIDA:aktif/pasif biasanya
Bersamaan dengan Na:(65% tub proks/25 %
Henle/10 % diantara tub distal-kolligen
REABSORBSI
KALIUM:
-50% diserap di tub prksimal/40 % pars
ascnden L/H /10 % dukt koligen
REABSORBSI ASAM AMINO:
-semua asam amino direabsorbsi tub
proksima
REABSORBSI PROTEIN PLASMA:
-<<< protein yang filtrasi di glomerulus
-Reabsorbsi di tubuli proksimal
REABSORBSI UREA:hasil akhir metabolis
Protei di hepar.(50 % tub proksimal/40 %
urea menetap filtratdiekresikan
REABSORBSI
BIKARBONAT:
@tubuli proksimal-aktif(Duk koligent<)
FUNGSI ENDOKRIN GINJAL:
@Renin
@1-25 dihidroksi vitamin D3mineralisasi tulang
@eritropoitin--merupakan respon dari iskhemia ginjal berfungsi
pembentukan sel-sel darah merah
Bahan
yang dipergunakan :
Inulin
PAH
Creatinin
Iotalamat radioaktif
FIGURE 167
Renal handling of three hypothetical substances X, Y, and Z. X is
filtered and secreted but not reabsorbed. Y is filtered, and a
fraction is then reabsorbed. Z is filtered and completely reabsorbed.
FIGURE 168
Forces involved in glomerular filtration. The symbol
denotes the osmotic force due to the presence of protein in
glomerular capillary plasma.
FIGURE 1610
Example of renal handling of inulin, a substance that is
filtered by the renal corpuscles but is neither reabsorbed nor
secreted by the tubule. Therefore, the mass of inulin
excreted per unit time is equal to the mass filtered during
the same time period, and as explained in the text, the
clearance of inulin is equal to the glomerular filtration rate.
FIGURE 1611
Control of the bladder.
Micturation
Reflex control
Voluntery control
Blader fills
Cereberal
Cortex
+
Strech reseptor
+
Parasymphatetic
nerve
+
Bladder
Bladder
contraction
Motor neuron to
external sphinter
External urethral
sphinter open when
motor neuron
inhibition
External urethara
sphinter remains
closed when motor
neuron is stimulated
No Urination
1.NITROGEN
UREA DARAH(BUN)
Urea produk akhir metabolisme protein dan
asam amino-mengandung nitrogen
Peningkatan BUN indikasi fungsi ginjal
menurun
BUN ditentukan :
-peningkatan/penurunan asupan protein
-cedra otot
-sakit hepar
-Rasio BUN : creatinin=peny hepar <10:1
atau > 15:1
2.Creatinin
PERUBAHAN
FILTRASI GLOMERULUS
@Perobahan P kapiler-MAP
@Perobahan tekanan koloid osmotik
plasma--kadar protein plasma
@Perubahan tekanan koloid cairan intertitial-kadar protein c.intertitial
@Perobahan tekanan cairan intertitial
AZOTEMIA :peningkatan abnormalbahan
sisa bernitrogen dalam
darah(urea/asam urat/kretinin
KONSEP PATOFISIOLGI
UREMIA
OSTEODISTROFI
GINJAL:demineralisasi
tulang akibat penyalit ginjal.
Sebab:-penurunan pengaktifan Vit D3
oleh ginjal
-penumpukkan ino pospat
-peranan tulang sebagai penyanggah H ion dalam plasma
ASIDOSIS METABOLIK(Asidosis ginjal) adalah
penurunan Ph plasma tidak disebabkan oleh
ggn pernafasan
ENSEFALOPATI UREMIK :perubahan neurologi
akibat penyakit ginjal yang parah
DIALISIS
1.Hipospadia/epispadia
2agenesis
ginjal
3.Refluks vesiko ureter/uretrovesikal
4.Batu ginjal
5.Kandung kemih neurogenik
6.Infeksi saluran kemih
7.Glomerulonefritis
8.Mioglobin urea
9.Sindroma Uremik Hemolitik
10.Gagal ginjal akut/kronik
Adalah
KOMPLIKASI
:
@disfungsi ejaklasi pada saat dewasa
@ekstrofia pemejanan melalui kulit
PENATALAKSANAAN :koreksi bedah
dilakukan sebelum anak umur 1-2 thn
AGENSIS GINJAL :kegagalan pembentukan
ginjal selama gestasi unilateral/bilateral:
KLINIK:
@bilateral agenesis ginjal(Sind Pooter)
biasanya meninggal inuterus/segera
lahir
@kompenssai ginjal yang sehat 2 X >
DIAGNOSTIK:
@ultrasound perinatal
@scan computerize axial tomogrphy(CAT)
PENTALAKSANAAN:
@bila ginjal yang ada sehat tdk
diperlukan
@Tindakan bedah
REFLUKS VESIKOURETER/URETROVISIKAL:
Adalah aliran balik urin dari vuueter
yang terjadi:kelainan
konggenital/neurogenik blader/infeksi
berulang-- jr parut
KLINIS:-infeksi
Adalah
kemih
Komponen pembentuk batu:magnesium/amonium/asam
urat/atau komonasi
Etiologi:-peningkatan/penurunan pH urin
-diet tetentu
-stasis urin
-fk risiko peninggkatan BB
KLINIS:
-Kolik renal/asimtomatik
-hematuria/produksi urin turun
-pengenceran urin
BATU GINJAL
DIAGNOSTIK:
-pemeriksaan darah/urin
-Radiografi/urografi intra vena
KOMPLIKASI:
-Obstruksi urin
-kollaps nefron/kapilerishkemia ginjal
atau gagal ginjal.
PENATALAKSANAAN:
-banyak minum
-modifikasi diet
-perubahan pH urin
-Litotripsi/tindakan bedah
Adalah
DIAGNOSTIK: