2 a.Bagaimana anatomi,fisiologi traktus urinarius feminina ?reyki,jaka,mira Ginjal merupakan organ berbentuk seperti kacang yang terletak di kedua sisi kolumna vertebralis. Ginjal kanan sedikit lebih rendah dibandingkan ginjal kiri karena tertekan ke bawah oleh hati. Kutub atasnya terletak setinggi iga ke duabelas, dan kutub atas ginjal kiri terletak setinggi iga ke sebelas. Kedua ureter mempunyai saluran yang panjangnya 25 hingga 30cm, terbentang dari ginjal sampai vesika urinaria. Fungsi satu satunya adalah menyalurkan urin ke vesika urinaria. Vesika urinaria adalah sesuatu kantong berotot yang dapat mengempis yang letaknya di belakang simphisis pubis dan mempunyai tiga muara, yaitu dua dari ureter dan satu menuju uretra. Uretra adalah saluran keci; yang dapat mengembang, berjalan dari vesika urinaria sampai keluar tubuh. Panjang sekitar 4cm. 1. Filtrasi Terjadi di glomerulus, proses ini terjadi karena permukaan afferent lebih besar dari permukaan efferent, maka terjadi penyerapan darah. Sebagian yang tersaring adalah bagian darah, kecuali protein. Cairan yang disaring ditampung oleh kapsula Bowman yang terdiri dari glukosa, air, sodium, sulfat, bikarbonat dan diteruskan ke tubulus ginjal. 2. Reabsorbsi Terjadi penyerapan kembali sebagian glukosa, sodium, klorida, fosfat, dan beberapa ion bikarbonat. Prosesnya terjadi secara pasif yang dikenal dengan obligator

reabsorbsi, terjadi pada tubulus atas. Pada tubulus ginjal bawah terjadi penyerapan dari sodium dan ion bikarbonat kembali, bila diperlukan akan diserap kembali ke dalam tubulus bawah. Penyerapan yang terjadi secara aktif dikenal sebagai reabsorbsi fakultatif dan sisanya dialirkan pada papilla renalis. 3. Sekresi Sekresi : perpindahan molekul dari CES ke lumen tubulus nefron. pada proses sekresi terjadi difusi zat dari kapiler peritubulus ke interstisium zat menuju lumen tubulus dengan menyebrangi tight junction antar sel (jalur paraselular) atau melewati membrane basolateral dan membrane apical (jalur transelular). 4. Eksresi Sisa penyerapan kembali yang terjadi pada tubulus diteruskan ke piala ginjal, selanjutnya diteruskan keluar. b.Apa penyebab kencing berkurang,bewarna keruh dan sekali-kali berbusa ?vidro,reyki,jaka

Causes of ProteinuriaMechanism Examples

Glomerular

Primary glomerular disorders (eg, membranous nephropathy, minimal change disease, focal segmental glomerulosclerosis) Secondary glomerular disorders (eg, diabetic nephropathy, preeclampsia, postinfectious glomerulonephritis, lupus nephritis, amyloidosis) Fanconi syndrome Acute tubular necrosis Tubulointerstitial nephritis Polycystic kidney disease Acute monocytic leukemia with lysozymuria Monoclonal gammopathy Multiple myeloma Myelodysplastic syndromes Fever Heart failure Intense exercise or activity Orthostatic

Tubular

Overflow

Functional

Unknown

Glomerular proteinuria results from glomerular disorders, which typically involve increased glomerular permeability; this permeability allows increased amounts of plasma proteins (sometimes very large amounts) to pass into the filtrate. Tubular proteinuria results from renal tubulointerstitial disorders that impair reabsorption of protein by the proximal tubule, causing proteinuria (mostly from smaller proteins such as immunoglobulin light chains rather than albumin). Causative disorders are often

accompanied by other defects of tubular function (eg, HCO3 wasting, glycosuria, aminoaciduria) and sometimes by glomerular pathology (which also contributes to the proteinuria). Overflow proteinuria occurs when excessive amounts of small plasma proteins (eg, immunoglobulin light chains produced in multiple myeloma) exceed the reabsorptive capacity of the proximal tubules. Functional proteinuria occurs when increased renal blood flow (eg, due to exercise, fever, high-output heart failure) delivers increased amounts of protein to the nephron, resulting in increased protein in the urine (usually < 1 g/day). Functional proteinuria reverses when renal blood flow returns to normal. Orthostatic proteinuria is a benign condition (most common among children and adolescents) in which proteinuria occurs mainly when the patient is upright. Thus, urine typically contains more protein during waking hours (when people are more often upright) than during sleep. It has a very good prognosis and requires no special intervention. c.Bagaiman patofisiologi berkurang,bewarna keruh dan sekali-kali berbusa ?pipit,vidro,reyki d. Apa makna dari berkurang,bewarna keruh dan sekali-kali berbusa ?arnida,pipit,vidro e. Mengapa kencing tersebut sesekali berbusa ?dian,arnida,pipit 3 a.Apa penyebab sakit kepala dan rasa berat pada tengkuk ?aan,dian,arnida b.Bagaimana patofisiologi kepala dan rasa berat pada tengkuk ?dienda,aan,dian c.Bagaimana hubungan kepala dan rasa berat pada tengkuk dengan kasus ? vera,dienda,aan 4 a.Apa itu hipertensi ?mira,vera,dienda b.Bagaimana patofisiologi hipertensi ?jaka,mira,vera c.Apa saja faktor pencetus hipertensi ?reyki,jaka,mira Obesitas Stress Konsumsi Alkohol Asupan garam berlebih Diabetes Perokok d.Apa dampak hipertensi sejak 3 tahun yang lalu ?vidro,reyki,jaka Hipertensi yang lama dapat melukai target organ ( umumnya sistem kardiovaskular, otak, dan ginjal) meningkatkan resiko Penyakit Arteri Koroner (CAD), Myocard Infark, stroke hemoragik, dan gagal ginjal) dengan cara perkembangan dari arteriolosclerosis. e.Apa itu kencing manis ?pipit,vidro,reyki f.Bagaimana patofisiolgi kencing manis ?arnida,pipit,vidro g.Apa saja faktor pencetus kencing manis ?dian,arnida,pipit

h.Apa dampak kencing manis 10 tahun yang lalu ?aan,dian,arnida i.Bagaimana hubungan kencing manis 10 tahun ang lalu dan hipertensi sejak 3 tahun yang lalu dengan kasus ?dienda,aan,dian j.Organ apa saja yang terlibat pada hipertensi ? vera,dienda,aan 5.Bagaimana interpretasi dan mekanisme pemeriksaan fisik ? a.TB : 155cm,BB : 65 tahun ,mira,vera,dienda b TD : 180/100mmHg,jaka,mira,vera c.Pemeriksaan jantung : kardiomegali.reyki,jaka,mira d.Pemeriksaan abdomen : ascites (+) minimal.vidro,reyki,jaka e.Pemeriksaan EKG : LVH.pipit,vidro,reyki 6.Bagaimana interpretasi dan mekanisme pemeriksaan laboratorium ? a.darah : Hb : 11gr%.arnida,pipit,vidro b.gula darah puasa : 110gr/dl.dian,arnida,pipit c.gula darah postprodial : 180/dl.aan,dian,arnida d.ureum : 65mg/dl.dienda,aan,dian e.kreatinin : 2,5 u/l.vera,dienda,aan f. Na : 140 mEg/l.mira,vera,dienda g.Ka : 4,7 mEg/l.jaka,mira,vera h. Urin : protein urin (+4).reyki,jaka,mira

Protein dipstick grading Designation Trace 1+ 2+ 3+ 4+ 520 mg/dL 30 mg/dL 100 mg/dL 300 mg/dL More than 2000 mg/dL Less than 0.5 g/day 0.51 g/day 12 g/day More than 2 g/day Approx. amount Concentration Daily

results from glomerular disorders, which typically involve increased glomerular permeability; this permeability allows increased amounts of plasma proteins (sometimes very large amounts) to pass into the filtrate i. Bagaimana cara pemeriksaan gula darah puasa dan postprandial ?vidro,reyki,jaka 7.Bagaimana cara mendiagnosis kasus ini ?pipit,vidro,reyki 8.Gangguan apa saja yang mungkin terjadi ?arnida,pipit,vidro 9.Bagaimana pemeriksaan penunjang ?dian,arnida,pipit 10.Bagaiamana diagnosis kerja ?aan,dian,arnida 11.Bagaiamana penatalaksanaannya ?dienda,aan,dian 12.Prognosis ?vera,dienda,aan 13.Komplikasi ?mira,vera,dienda 14.Etiologi ?jaka,mira,vera 15.Epidemiologi ?reyki,jaka,mira Prevalensi gagal ginjal yang disebabkan nefropati diabetik di Amerika Serikat yaitu 40% pada penderita diabetes melitus tipe 1 dan 20%-30% pada penderita diabetes melitus tipe 2

16.KDU.vidro,dian,reyki,jaka 3a. Mampu membuat diagnosis klinik berdasarkan pemeriksaan fisik dan pemeriksaan pemeriksaan tambahan yang diminta oleh dokter (misalnya : pemeriksaan laboratorium sederhana atau X-ray). Dokter dapat memutuskan dan memberi terapi pendahuluan, serta merujuk ke spesialis yang relevan (bukan kasus gawat darurat). 17.Pandangan islam mengenai pola hidup sehat ?pipit,vidro,reyki Janji Allah diberikan kepada orang yang berpuasa ditegaskan dengan sabda Nabi Muhammad SAW yang diriwayatkan oleh Ibnu Suny dan Abu Nuaim: Berpuasalah maka anda akan sehat.

IV.Hipotesis Rosa,perempuan 51 tahun mengeluh sembab pada kedua tungkai dan lengan disebabkan karena nefropati et causa hipertensi dan DM. V.learning issue 1.Anatomi dan fisiologi traktus urinarius feminina.vidro,vera,arnida 2.DM.pipit,mira,dian 3.hipertensi.arnida,jaka,aan 4.nefropati.dian,reyki,dienda 5.EKG.aan,vidro,vera 6.pandangan islam.dienda,pipit,mira

DIABETIC NEPHROPATHY (See also Diabetes Mellitus and Disorders of Carbohydrate Metabolism: Diabetic nephropathy.) Diabetic nephropathy (DN) is glomerular sclerosis and fibrosis caused by the metabolic and hemodynamic changes of diabetes mellitus. It manifests as slowly progressive albuminuria with worsening hypertension and renal insufficiency. Diagnosis is based on history, physical examination, urinalysis, and urine albumin/creatinine ratio. Treatment is strict glucose control, angiotensin inhibition (ACE inhibitors or angiotensin II receptor blockers), and control of BP and lipids. DN is the most common cause of nephrotic syndrome in adults and of end-stage renal disease in the US, accounting for up to 80% of cases of the latter. The prevalence of renal failure is probably about 40% among patients with type 1 diabetes mellitus. The prevalence of renal failure among patients with type 2 diabetes mellitus is usually stated as 20 to 30%, but this figure is probably low. Renal failure is particularly common in certain ethnic groups, such as blacks, Mexican-Americans, Polynesians, and Pima Indians. Other risk factors include the following: Duration and degree of hyperglycemia Hypertension Dyslipidemia Cigarette smoking

Certain polymorphisms affecting the renin-angiotensin-aldosterone axis Family history of diabetic nephropathy Genetic variables (decreased number of glomeruli) Renal failure usually takes 10 yr after the onset of nephropathy to develop; however, because type 2 diabetes is often present for several years before being recognized, nephropathy often develops < 10 yr after diabetes is diagnosed. Pathophysiology Pathogenesis begins with small vessel disease. Pathophysiology is complex, involving glycosylation of proteins, hormonally influenced cytokine release (eg, transforming growth factor-), deposition of mesangial matrix, and alteration of glomerular hemodynamics. Hyperfiltration, an early functional abnormality, is only a relative predictor for the development of renal failure. Hyperglycemia causes glycosylation of glomerular proteins, which may be responsible for mesangial cell proliferation and matrix expansion and vascular endothelial damage. The GBM classically becomes thickened. Lesions of diffuse or nodular intercapillary glomerulosclerosis are distinctive. There is marked hyalinosis of afferent and efferent arterioles as well as arteriosclerosis; interstitial fibrosis and tubular atrophy may be present. Only mesangial matrix expansion appears to correlate with progression to end-stage renal disease.

Diabetic Nephropathy (Mesangial Cell Proliferation and Matrix Expansion)

Diabetic Nephropathy (Nodules)

Diabetic Nephropathy (Hyalinosis)

DN begins as glomerular hyperfiltration (increased GFR); GFR normalizes with early renal injury and mild hypertension, which worsens over time. Microalbuminuria, urinary excretion of albumin in a range of 30 to 300 mg albumin/day, then occurs. Urinary albumin in these concentrations is called microalbuminuria because detection of proteinuria by dipstick on

routine urinalysis usually requires > 300 mg albumin/day. Microalbuminuria progresses to proteinuria > 0.5 g/day at a variable course, usually over years. Nephrotic syndrome (proteinuria 3 g/day) precedes end-stage renal disease, on average, by about 3 to 5 yr, but this timing is also highly variable. Other urinary tract abnormalities commonly occurring with DN that may accelerate the decline of renal function include papillary necrosis, type IV renal tubular acidosis, and UTIs. In DN, the kidneys are usually of normal size or larger. Symptoms and Signs DN is asymptomatic in early stages. Sustained microalbuminuria is the earliest warning sign. Hypertension and some measure of dependent edema eventually develop in most untreated patients. In later stages, patients develop symptoms and signs of uremia (eg, nausea, vomiting, anorexia) earlier (ie, with higher GFR) than do patients without DN, possibly because the combination of end-organ damage due to diabetes (eg, neuropathy) and renal failure worsens symptoms. Diagnosis Screening of all patients with diabetes with random urine albumin/creatinine ratio Urinalysis for signs of other renal disorders (eg, hematuria, RBC casts) The diagnosis is suspected in patients with diabetes who have proteinuria, particularly if they have diabetic retinopathy (indicating small vessel disease) or risk factors for DN. Other renal disorders should be considered if there are any of the following: Heavy proteinuria with only a brief history of diabetes Absence of diabetic retinopathy Rapid onset of heavy proteinuria Gross hematuria RBC casts Rapid decline in GFR Small kidney size Urinary protein: Patients are tested for proteinuria by routine urinalysis; if proteinuria is present, testing for microalbuminuria is unnecessary because the patient already has macroalbuminuria suggestive of diabetic renal disease. In patients without proteinuria on urinalysis, an albumin/creatinine ratio should be calculated from a mid-morning urine specimen. A ratio 0.03 mg/mg ( 30 mg/g) indicates microalbuminuria if it is present on at least 2 of 3 specimens within 3 to 6 mo and if it cannot be explained by infection or exercise. Some experts recommend that microalbuminuria be measured from a 24-h urine collection, but this approach is less convenient, and many patients have difficulty accurately collecting a specimen. The random urine albumin/creatinine ratio overestimates 24-h collection of microalbuminuria in up to 30% of patients > 65 due to reduced creatinine production from reduced muscle mass. Inaccurate results can also occur in very muscular patients or if vigorous exercise precedes urine collection. For most patients with diabetes who have proteinuria, the diagnosis is clinical. Renal biopsy can confirm the diagnosis but is rarely necessary. Screening: Patients with type 1 diabetes without known renal disease should be screened for proteinuria and, if proteinuria is absent on routine urinalysis, for microalbuminuria, beginning 5 yr after diagnosis and at least annually thereafter.

Patients with type 2 diabetes should be screened at the time of diagnosis and annually thereafter. Prognosis Prognosis is good for patients who are meticulously treated and monitored. Such care is often difficult in practice, however, and most patients slowly lose renal function; even prehypertension (BP 120 to 139/80 to 89 mm Hg) or stage 1 hypertension (BP 140 to 159/90 to 99 mm Hg) may accelerate injury. Systemic atherosclerotic disease (stroke, MI, peripheral arterial disease) predicts an increase in mortality. Treatment Maintenance of glycosylated Hb (HbA1c) 7.0 Aggressive BP control, beginning with angiotensin inhibition Primary treatment is strict glucose control to maintain HbA1c 7.0; maintenance of euglycemia reduces microalbuminuria but may not retard disease progression once DN is well established. Glucose control must also be accompanied by strict control of BP to < 130/80 mm Hg. Some experts suggest BP should be 110 to 120/65 to 80 mm Hg, particularly in patients with protein excretion of > 1 g/day; however, others claim that BP values < 120/85 mm Hg are associated with increased cardiovascular mortality and heart failure. Dyslipidemia should also be treated. Angiotensin inhibition is first-line therapy. Thus, ACE inhibitors or angiotensin II receptor blockers are the antihypertensives of choice; they reduce BP and proteinuria and slow the progression of DN. ACE inhibitors are usually less expensive, but angiotensin II receptor blockers can be used instead if ACE inhibitors cause persistent cough. Treatment should be started when microalbuminuria is detected regardless of whether hypertension is present; some experts recommend drugs be used even before signs of renal disease appear. Diuretics are required by most patients in addition to angiotensin inhibition to reach target BP levels. Dose should be decreased if symptoms of orthostatic hypotension develop or serum creatinine increases by more than 30%. Nondihydropyridine Ca channel blockers (diltiazem SOME TRADE NAMES CARDIZEM CARTIA DILACOR Click for Drug Monograph and verapamil SOME TRADE NAMES CALAN ISOPTIN Click for Drug Monograph ) are also antiproteinuric and renoprotective and can be used if proteinuria does not meaningfully decrease when target BP is reached or as alternatives for patients with

hyperkalemia or other contraindications to ACE inhibitors or angiotensin II receptor blockers. In contrast, dihydropyridine Ca channel blockers (eg, nifedipine SOME TRADE NAMES ADALAT PROCARDIA Click for Drug Monograph , felodipine SOME TRADE NAMES PLENDIL Click for Drug Monograph , amlodipine SOME TRADE NAMES NORVASC Click for Drug Monograph ) are relatively contraindicated because they may worsen proteinuria and renal function. ACE inhibitors and nondihydropyridine Ca channel blockers have greater antiproteinuric and renoprotective effects when used together, and their antiproteinuric effect is enhanced by Na restriction. Nondihydropyridine Ca channel blockers should be used with caution in patients taking -blockers. Dietary protein restriction yields mixed results. The American Diabetic Association recommends that people with diabetes and overt nephropathy be restricted to 0.8 g protein/kg/day. Significant protein restriction should be done only with close dietary monitoring to ensure a balanced supply of amino acids, because undernutrition may be a significant risk. Kidney transplantation with or without simultaneous or subsequent pancreas transplantation (see Transplantation: Kidney Transplantation) is an option for patients with end-stage renal disease. The 5-yr survival rate for patients with type 2 diabetes receiving a kidney transplant is almost 60%, compared with 2% for dialysis-dependent patients who do not undergo transplantation (though this statistic probably represents significant selection bias). Renal allograft survival rate is > 85% at 2 yr. http://www.merckmanuals.com/professional/genitourinary_disorders/glomerular_disorders/ nephrotic_syndrome.html#v1056071