Sunum yükleniyor. Lütfen bekleyiniz

Sunum yükleniyor. Lütfen bekleyiniz

1. Structural overview 2. Functional overview 3. Clinical features of kidney disease 4. Laboratory investigations.

Benzer bir sunumlar


... konulu sunumlar: "1. Structural overview 2. Functional overview 3. Clinical features of kidney disease 4. Laboratory investigations."— Sunum transkripti:

1

2 1. Structural overview 2. Functional overview 3. Clinical features of kidney disease 4. Laboratory investigations

3

4 nephron  The nephron is the basic unit of the kidney –  Each kidney has – nephrons. glomerulus tubule  A nephron consists of the glomerulus and the associated tubule that leads to the collecting duct.  Urine is formed by filtration in the glomerulus; it is then modified in the tubules by the reabsorption and secretion of substances

5

6

7

8 Homeostasis The kidney is one of the major organs involved in whole- body homeostasis. Among its homeostatic functions arehomeostasis  acid-base balance,  regulation of electrolyte concentrations,electrolyte  control of blood volume, and regulation of blood pressure.blood volumeblood pressure The kidneys accomplish these homeostatic functions independently and through coordination with other organs, particularly those of the endocrine system. The kidney communicates with these organs through hormones secreted into the bloodstream.endocrine system

9  Acid-base balance The kidneys regulate the pH of blood by adjusting H+ ion levels, referred as augmentation of mineral ion concentration, as well as water composition of the blood.pH

10  Blood pressure - Renin-angiotensin system Renin-angiotensin system Sodium ions are controlled in a homeostatic process involving aldosterone which increases sodium ion reabsorption in the distal convoluted tubules.aldosterone

11

12  Plasma volume Any significant rise or drop in plasma osmolality is detected by the hypothalamus, which communicates directly with the posterior pituitary gland. A rise in osmolality causes the gland to secrete antidiuretic hormone, resulting in water reabsorption by the kidney and an increase in urine concentration. The two factors work together to return the plasma osmolality to its normal levels.plasma osmolality hypothalamusposterior pituitary gland antidiuretic hormone

13  Excretion of waste products The kidneys excrete a variety of waste products produced by metabolism, including the nitrogenous wastes:metabolism urea urea (from protein catabolism) and uric aciduric acid (from nucleic acid metabolism)

14  Hormone secretion The kidneys secrete a variety of hormones, including: hormones renin, erythropoietinerythropoietin, vitamin Dvitamin D.

15 Regulation e.g. homeostasis, water, acid/base Excretion e.g. urea, creatinine Endocrine e.g. renin, erythropoietin, 1,25 dihydroxycholecalciferol- conversion only in kidney!

16

17

18

19 ACUTE RENAL FAİLURE  Prerenal acute renal failure  Intrinsic acute renal failure  Postrenal renal failur Chronic renal failure

20  Prerenal acute renal failure haemorrhage, fluid loss, cardiac failure or hypotension that leads to renal hypoperfusion and a decrease in GFR

21  Intrinsic acute renal failure Many cases are due to nephrotoxic drugs (aminoglycosides and non-steroidal anti- inflamatory drugs) Renal ischaemia (following severe blood loss or hypotension) leading to acute tubuler necrosis

22  Postrenal renal failure  Obstruction to the flow of urine leads to an increase in hydrostatic pressure, which acts in opposition to glomerular filtration and, if prolonged, leads to secondary renal tubular damage.  Causes of obstruction include renal calculi, prostatic enlargement (hypertrophic or neoplastic), other neoplasms of the urinary tract.

23  Chronic renal failure  Many disease processes (glomerulonephritis, Diabetes mellitus, hypertansion, pyelonephritis and polycystic kidneys) can lead to progressive, irreversible impairment of renal function.  Chronic renal failure develops insidiously, often over many years, and is irreversible, leanding eventually to end-stage renal failure.  Patients with end-stage renal failure require either long-term renal replacement treatment (i.e., dialysis) or a successful renal transplant in order to survive.

24  detect renal damage  monitor functional damage  help determine etiology

25

26

27

28  Urinalysis by test strips  Serum Creatinine or Urea /BUN(blood urea nitrogen)  Creatinine clearance  Urinary proteins  Urinary stones tests

29 Diseases affecting the kidneys can selectively damage glomerular or tubuler function

30 The principal function of the glomeruli is to filter water and low molecular weigh components of the blood and retaining cells and high molecular weigth components

31  Laboratory tests of renal function  Urinalysis by test strips –  Tests of glomerular filtration rate  Tests of renal tubular function

32 Urinalysis by test strips Now a really easy, cheap, sensitive, routine way of testing subjects, but not good enough on its own and not quantitative

33  Oligouria – excrete < 300 ml/day. › Might be “physiological” as in hypotension or hypovolaemia where we compensate, but more often due to renal disease or obstructive nephropathy.  Polyuria – persistent, large increase in urine output associated with nocturia. › Must distinguish from higher frequency of small volumes of urine. › Usually due to hysterical intake of water, increased excretion of solute (e.g. hyperglycaemia/glycosuria), defect in concentrating ability or ADH failure).  Osmolality – useful for determining whether ionic imbalances exist in subject. › May indicate renal failure (e.g. excess urea) or problems with ADH.  Urinary pH – mainly for acidosis/alkalosis determination – important when studying metabolism of various nutrients e.g. glucose during exercise

34  Blood – very sensitive – 2 or more cells can produce result. › Sometimes TOO sensitive, giving false positives. › Can’t distinguish between blood and free Hb, so usually double- check with microscope.  Protein › Strips detect 100 mg/l or more in urine – react with albumin. › Check throughout 24 hr period › Some protein always excreted, but can be falsely increased by exercise, growth, fever etc. › Time of day taken – lying down causes protein to settle and it’s not detected in urine.  Glucose › Positive test can mean diabetes mellitus. › Have to exclude ingestion of high sugar diet.

35

36

37  Clean, mid-stream sample needed.  White cells › 10 or more WBC’s per cm 3 indicates inflammation (e.g. urinary tract infection)  Red cells – again, subject may be aware of it already via pain.  Casts › Cylindrical bodies made from precipitated proteins, often seen normally after exercise. › Red cell casts (even one) always means disease.  Bacteria – allows you to decide which antibiotic is best for subject. Checking for blood/urine not always good for checking for infections, since these subjects can have completely clear urine

38  Üriner yolun son kısmı olan üretra ve kadında vagina kontaminasyonu kaynaklıdır.İdrarda en yaygın bulunan epitel hücreleridir  Çok büyük olup (idrar mikroskopisinde görülen en büyük hücre), küçük (hücreye göre çok küçük) ve tek çekirdekli, iri sitoplazmalı, yassı, düzensiz sınırları bulunan hücrelerdir. Bazılarında çift çekirdek görülebilir  İdrarda her sahada 5 adet bulunması normal kabul edilir  Vaginal kontaminasyon, idrar örneğinin cilt florası ile muhtemel kontaminasyonu, Üretrovaginal/ üretrovezikal fistül, Üretrit gibi durumları düşündürmelidir  Epitel Hücreleri Squamoz epitelyal hücreler:

39  Böbrek korteks ve medullasındaki tübülleri oluşturan epitelden kaynaklıdır.  Küçük, yuvarlak, çok köşeli (poliglonal) dir. Lökositlerden biraz büyük olup, granüler ve yassı epitel hücresine göre büyük bir çekirdeği bulunur.  Dansitesi düşük bir idrarda lökositlere çok benzer. Nefrotik sendrom ve akut tübüler hasarda idrardaki sayıları artar.  İdrarda normalde bulunmaz. Lökositlerle karışabilir. Ancak Lökositten daha büyüktürler. Yukarıdaki resimde likosit ve tübüler epitel bir arada görülüyor. Renal Tübüler Epitelyal Hücreler

40  Böbrek pelvisinden üretra çıkışına kadar üriner sistemin büyük çoğunluğunun iç yüzeyini döşeyen epitelden kaynaklanır.  Daha düzenli ve hücre sınırları mevcuttur. Merkezi nükleuslu, füsiform (sferik, poliheral, iğ şeklinde, armudumsu, değişik şekillerde) sitoplazmalı epiteldir. Mesaneden gelenler daha çok köşeli-iri - pul gibidir.  İdrarda her sahada 5 adet bulunması normal kabul edilir. İdrarda her sahada 5 den fazla bulunması na değişici epitel (transisyonel epitelüri) atılımı denir. Üriner sistem inflamatuar hastalıklar,travmaya bağlı (sistoskopi) ve mesane kanserinde artabilir. 

41  İdrarda en sık bulunan silendirdir. Saydam, renksizdir. Işık kontrast hale getirilince daha kolay görülür  Hyalen silendirlerin klinikte önemleri fazla değildir. Klinik değeri azdır. Her sahada 2 tane bulunması normal kabul edilir.Ancak; genişse böbrek tubulus hastalıklarını gösterir. Ayrıca idrarda devamlı görülmesi organik böbrek has. gösterir.  Akut nefritik sendrom, akut glomerulonefrit ve nefrotik sendromda rastlanabilir. Asit idrarda, konsantre idrarda ve diüretik tedavisinde, dehidratasyonda ve normalde görülebilirler.

42  Hiyalen silendire eritrosit girmesiyle oluşur.  İdrarda normalde bulunmaz.  Eritrosit silendir aşikar bir glomerül lezyonunu ve özellikle aktif bir glomerülonefriti gösterir. Akut nefritik sendrom (akut glomerülonefrit ve diğerleri) için tipiktir. 

43  Hiyalen silendire lökosit girmesiyle oluşur. Bazen lökositler; parçalar halinde, kümeler şeklinde, deforme şekilde bulunur.  Bol piyüri ile beraber görülürse piyelonefrit veya tübülointerstisyel hastalık için karakteristiktir. Eritrosit silendiri ile beraber görüldüğünde glomerülonefrit düşünülmelidir. 

44  Hiyalen silendire epitel girmesiyle oluşur. Burada ufak bir hatırlatma yapmakta yarar var: silendirler tübülüslerde oluşur, bu yüzden yapısına sadece renal tübüler epitel girebilir, tübülüslerin altında lokalize olan transisyonel epitel ya da yassı epitel asla sediment yapısına giremez  Tubulusları (tubuler epitel hücreleri) etkileyen olaylarda görülür.  Viral enf.  Akut piyelonefrit  ABY-ATN  Amiloidoz  Ağır metal toksikasyonunda görülür. 

45  Anlamlı proteinürili hastalar arasında epitelyal silendir içindeki hücrelerin Dejenerasyonu karakteristik „maltese cross“ görünümüne ve yağ silendirlerine neden olabilir. Bu damlacıklar kolesterol ve kolesterol esterlerinden oluşur.  Nefrotik senromda görülür. 

46  Homojen, granüler, yoğun, düz, silendirik yapıdadır. Şekli ve büyüklüğü hiyalin silendire benzer ama şeffaf- mat değildir, granüllüdür. Görünümüne göre iki tiptir: İnce granüllü silendirler: Granüller küçük ve düzenlidir. Işığı az kırar. Kaba granüllü silendirler: Granüller büyük ve düzensizdir (irregüler). Işığı çok kırar. Hücresel hasarı göstergesidir  Nefrotik, nefritik sendrom ve glomerülonefritlerde görülür. Silendirler daha önce var olan hücre silendirlerinde eritrosit, lökosit veya epitellerin dejenere olup parçalanması sonucunda oluşurlar. 

47

48  En sık görülen kristal oluşumudur. pH=6-7 civarında oluşur.  Renksizdir.  İki şekli bulunur: Dihidrat şekli: Mektup zarfı şeklindedir.Daha sık rastlanır.Monohidrat şekli: Yuvarlak, halter şeklindedir. Daha nadir rastanır. İdrarda normalde bulunabilir.  Klinikle uyumlu görülmesi patolojik sayılabilir. Ispanak- portakal- domates-sarımsak- asparagus- meyan kökü gibi okzalik asit yönünden zengin besinler alındığında görülür. Yüksek doz askorbik asid alımında Taş: Taze idrarda kümeler halinde olup eritrosit ve lökosit ile beraber görülürse önem taşır.DM, karaciğer has, kalp has, akc. has artar

49  Sarımtrak- renksizdir. Tabut kapağı şeklindedir. X harfi- tavuk tüyüne benzer şekilde de görülebilir.  Bakteriyel artışla birliktedir. Üriner stazda (Prostat büyümesi) Kronik enf. (kronik sistitde)

50  Amorf şekilde görülür. Büyük kümeler haline ince granüller şeklinde görülür.  Santrifüj sonrası tüpün dibinde beyaz bir çökelek oluşur  Görüldüğü duruml Yüksek ateş Sıvı kaybı

51  Renksizdir. Geniş- ince- düzensiz- noktalı tabakalar şeklindedir. Geniş plaklar şeklinde de olabilir.  Prizmalar birleşerek rozet veya yıldız şeklinde görülebilir (Yıldızı gibi fosfatlar da denir).  Görüldüğü durumlar  Kronik sistit  Prostat hipertrofisinde 

52  Sarı- kahverengi renkte veya renksizdir.  Kama, halter, baklava, prizmatik rozetler, kübik, oval, düzensiz- hexagonal tabakalar halinde görülebilir.  Santrifüj sonrası tüpün dibinde pembe bir çökelti oluşturur  İdrarda normalde bulunabilir. Klinikle uyumlu olarak görülmesi patolojik sayılabilir.  Görüldüğü durumlar:  - Taş (Taze idrarda bulunması teşhisi açısından önemli olabilir kümeler halide saptanırsa böbrek- mesanede taş göstergesidir)  - Gut  - Akut ateşli hastalıklar  - Kronik nefritik sendrom

53  Renksiz - hexagonaldir (6 köşeli). Refraktildir. Taze idrarda biraraya gelme eğilimdedir.  İdrarda normalde bulunabilir.  Klinikle uyumlu görülmesi patolojik sayılabilir. Sistinüri denir.  Görüldüğü Durumlar:  - Konjenital sistinüri (Klinik olarak tek anlamlı kristalüridir)  - Wilson hastalığı 

54  BİLURİBİN KRİSTALİ  Sarı- kırmızı- kahverengi renktedir. Baklava, iğne, granüler şekilinde görünür.  Biluribin yüksekliği olan durumlarda: Obs. Sarılık, karaciğer kanseri, karaciğer sirozu, tifo, kızıl, fosfor zehirlenmesinde görülür. 

55  ÜRAT KRİSTALLERİ  Sarı-pembe- turuncu (tuğla rengi) renktedir.  İdrarda normalde bulunabilir.Yüksek ateş, sıvı kaybında da olabilir 

56  SODYUM ÜRAT KRİSTALİ  Sarı-kahverenkli renksizdir.Amorf veya kristal şekilde olabilir.Yelpaze, ince uzun prizmalar şeklindedir.  İdrarda normalde bulunabilir.  Ateşli hastalıklar durumlarında da görülebili

57  KOLESTEROL KRİSTALİ  Renksizdir. Bir- birkaç köşesi kesik veya çentikli, geniş, yassı dikdörtgen tabakalar şeklinde görülür.  İdrarda normalde bulunabilir  - Dondurulmuş- beklemiş idrarda.  - Nefrotik sendrom  - Lenfatik obs.  - Lipoid nefroz, membranöz glomerülonefrit  - Sistit, pyelit gibi hastalıklarda görülür. 

58  KALSİYUM SÜLFAT KRİSTALİ  Uzun renksiz iğneler- uzun prizmalar şeklinde görülür.  Klinik önemi yoktur 

59

60  Urinalysis can be done macroscopically, biochemically microscopically (urinary sediment)

61 If there is poor renal function, you might expect any one of: Hyperkalaemia Decreased bicarbonate – poor filtration or acid/base disorders Elevated urea Elevated creatinine Elevated uric acid Hypocalcaemia Hyperphosphataemia pH – acid/base disorders pCO 2 away from 40mmHg – acid/base disorders Hypernatraemia These are the most common plasma constituents we would measure if we were analysing renal function in the lab. Cheap, easy, routinely done, and provide a large amount of information quickly.

62

63  = BUN (blood urea nitrogen)  Urea: product of protein catabolism  Synthesized by liver, majority excreted by kidney, partially reabsorbed in tubuli  Plasma concentration increases with decreased GFR

64 Serum UREA/BUN  Urea production is rapidly affected by protein intake. It fluctuates more widely than creatinine.  When protein catabolism is increased, urea rises rapidly as in haemorrhage in the bowels or body tissues, severe infections, burns, muscle injury, ingestion of steroids and tetracycline  Urea level falls with a low protein diet, starvation and liver damage.

65  BUN (Blood Urea Nitrogen)  Urea MA=60g/mol (%28 N)  60/28=2.14  Urea / 2.14 = BUN BUN x 2.14 = Urea  Normal range BUN – 8-20 mg/dl Urea – mg/dl

66  BUN influenced by diet and hormones, so it is NOT as good an indicator of renal function as serum creatinine levels  BUN increased in kidney disease, high protein diet, and after administration of steroids  BUN decreased in starvation, pregnancy and in persons on a low protein diet

67 Creatine: main storage compound of high energy phosphate needed for muscle metabolism. Creatinine: anhydride of creatine! CreatineCreatinine (Waste product) H2O

68  Best test for overall kidney function; not affected by diet or hormone levels  Waste product of muscle metabolism  Serum creatinine rises when kidney function is impaired Male mg/dL, Female mg/dL

69 Normal GFR ml/min/1.73 m2

70

71 Clearance is theoretical concept and is defind as the volume of plasma from which a measured amound of substance can be completely eliminated (cleared) into the urine per unit of time. This depends on the plasma concetration and excretory rate, wich, in turn, involve the glomerular filtration rate (GFR) and plasma flow.

72 GFR is the most widely used test of renal function. Ideally, it is measured using a substance which is: Eliminated only by the kidney Completely filtered from the blood by the glomeruli is not secreted, reabsorbed or metabolized by the renal tubules. Easily and accurately measured Glomerular filtration rate(GFR) Clearance test

73 Its accuracy is therefore a gold standard. Its accuracy is therefore a gold standard. The volume of blood from which inulin is cleared or completely removed in one minute is know as the inulin clearence and is equal to the GFR. The volume of blood from which inulin is cleared or completely removed in one minute is know as the inulin clearence and is equal to the GFR. GFR as measured by inulin clearance is a research tool. GFR as measured by inulin clearance is a research tool. Measurement of İnulin clearence requires the infusion of inulin into the blood and is not suitable for routin clinical use. Measurement of İnulin clearence requires the infusion of inulin into the blood and is not suitable for routin clinical use.

74  The most frequently used clearance test is based on the measurement of creatinine.  This endogenous substance is derived mainly from the turnover of creatine in muscle and daily production is relatively constant.  A small amount of creatinine is derived from meat in the diet.  There is a slight amount secreted by the tubules but common methods slightly overestimate plasma concentration.  A 24-hour urine collection is necessary. This urine specimen is also useful for quantitation of urinary protein.  The GFR varies inversely with the plasma concentration.

75

76 Clearance formula Creatinine(urine) C (mL/min/1.73m2) = Creatinine(urine) Creatinine(serum) x 1.73 A C = clearance in mL per min V = urine quantity per collection time A = body surface area in surface area in sguare meters Referans Range = Man 120 mL/min/1.73m2 Women 100 ml/min/1.73 m2 x V

77 CLEARANCE = U x V S U = concentration of creatinine in urine S = serum creatinine concentration V = urine quantity per collection time

78

79 Test protocol 1. 5 ml of blood is collected for the determination of creatinine 2. A 24-hour urine sample is collected. The collection period of the 24-h urine sample includes one daytime period and one nighttime period. 3. The creatinine concentration is determined in the collected urine sample 4. The clearence value is calculated. Besides the volume of urine collection, the height and body weight of the patient need to be known as well. Clearance results are related to 1.73 m2 body surface area of a person weighing 75 kg. The patient’s body surface area is derived from a nomogram, using his height and body weight.

80  Adults: 1.5 L/24 h typical in health,  oliguria < 400 mL,  anuria < 100 mL,  polyuria > 3000 mL

81  Absence of significant proteinuria is a sign of renal integrity and its presence indicates renal disease. In normal individuals the 24-hour urinary protein is less than 150 mg per day. Proteinuria could be due to:  Increased glomerular filtration because of increased permeability of basement membrane  Decreased reabsorption of proteins.  Addition of protein to urine (renal tubular cells, lymphatics, genitalia). In Bence Jones proteinuria, there are abnormal light chains which coagulate on heating at a temperature of 45" to 55°C and redissolve on boiling.

82 Creatinine + alkaline picrate solution Bright orange/red colored complex absorbs light at 485nm (many interfering substances in blood Can be minimized using rate method)

83  Plasma b2-microglobulin  B2-microglobulin is a small peptid.  İt is present on the surface of the most cells and in low concentrations in the plasma.  İt is completely filtered by the glomeruli and is reabsorbed and catabolized by proximal tubular cells.  Measurement of b2-microglobulin excretion provides a sensitive method of assesing tubular integrity.

84  Cystatin C  This low molecular weight peptide is produced by all nucleated cells.  İt is cleared from the plasma by glomerular filtration and its plasma concentration reflects the GFR.

85

86

87

88

89

90

91

92

93

94

95

96


"1. Structural overview 2. Functional overview 3. Clinical features of kidney disease 4. Laboratory investigations." indir ppt

Benzer bir sunumlar


Google Reklamları