TUBULAR INTERSTITIAL DISEASE

Question 1

TWO MAJOR PROCESSES

Answer 1

ISCHEMIC/TOXIC-AKI&ARF

INFLAMMATORY-TIN

Question 2

ACUTE TUBULAR INJURY

Answer 2

ACUTE REDUCTION OF RENAL FUNCTION AND MORPHOLOGIC EVIDENCE OF TUBULAR INJURY

Question 3

ACUTE TUBULAR INJURY CAUSES

Answer 3

ISCHAEMIC:
MALIGNANT HYPERTENSION 
MICROSCOPIC POLYANGITIS
MICROANGIOPATHIES
SYSTEMIC CONDITIONS ASSOCIATED WITH THROMBOSIS
HYPOVULEMIC SHOCK

DIRECT TOXIC INJURY
ENDOGENOUS(MYOGLOBIN,HAEMOGLOBIN,MONOCLONAL LIGHT CHAINS,BILE/BILIRUBIN)
EXOGENOUS(DRUGS,RADIOCONTRAST DYES,HEAVY METALS,ORGANIC SOLVENTS)

Question 4

ACUTE TUBULAR INJURY PATHOGENESIS

Answer 4

TUBULAR INJURY

PERSISTANT AND SEVERE DISTURBANCES IN BLOOD FLOW

Question 5

TUBULE CELL INJURY

Answer 5

SENSITIVE TO ISCHEMIA AND PRONE TO TOXINS BECAUSE:
LARGE SA
INCREASED 02 DEMAND AND HIGH METABILIC RATE
ACTIVE TRANSPORT
CONCENTRATE AND RESOPT TOXINS

Question 6

ISCHEMIA EFFECT ON TUBULE CELL

Answer 6

REDISTRIBUTION OF MEMBRANE PROTEINSLOSS OF CELL POLARITY
LATTER INCITES VASOCONSTR
TC EXPRESS CYTOKINES AND ADHESION MOLECULES,RECRUITING LEUKOCYTES
LUMINAL OBSTRUCTION
DECREASED GFR

Question 7

CLINICAL COURSE

Answer 7

INITIATING PHASE
LAST ABOUT 36 HRS
DOMINATED BY INCITING EVENT(SURGICAL,MEDICAL,OBSTRETIC)
SLIGHT DECLINE IN URINE OUTPUT AND RISE IN BUN

MAINTENAN
DOMINATED BY PERSISTANT RENAL FAILURE
DECREASE URINE OUTPUT 40-400MLS/DAY(OLIGURIC)

RECOVERY
RISING URINE OUTPUTAND POSSIBLY HYPOKALAEMIA -33/DAY
PROGNOSIS DEPENDS ON PART OF THE CAUSE OF THE ATN
IN SHOCK RELATED TO SEPSIS,BURNS OR OTHER MULTIORGAN FAILURE,MORTALITY>50

Question 8

ISCHAEMIC ACUTE TUBULAR NECROSIS

Answer 8

STRAIGHT PORTION OF THE PROXIMAL TUBULE & ASCENDING THICK LIMB
FOCAL LESIONS MAY ALSO OCCUR ON DISTALOFTEN IN CONJUCTION WITH THE CAST
EOSINOPHILIC HYALINE CASTS,PIGMENTED GRANULAR CASTS
CASTS :TAMM HORSFALL PROTEIN
INTERSTITIAL OEDEMA&ACC OF LEUKOCYTES
EPITHELIAL REGENERATION,FLATTENED EP CELLS WITH HYPERCHROMATIC NUCLEI&MITOTIC FIGURES

Question 9

TOXIC ACUTE

Answer 9

MOST OBVIOUS IN PCT
NECROSIS MAY BE NON SPECIFIC
MERCURIC CHLORIDE-SEVERLY INJURED CELLS CONTAIN LARGE ACIDOPHILIC INCLUSIONS.LATER WILL BE NECROTIC &CALCIFIED
CARBON TETRACHLORIDE POISONING-ACCNEUTRAL LIPIDS IN INJURED CELLS ,FOLLOWED BY NECROSIS
THYLENE GLYCOL-PRODUCE MARKED BALLOONING AND HYDROPIC /VACUOLAR DEGENERATION OF PCT.

Question 10

TUBULO-INTERSTITIAL NEPHRITIS

Answer 10

ACUTE AND CHRONIC