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Year2 Renal > Exam 2 Tubular and Interstitial Diseases > Flashcards

Exam 2 Tubular and Interstitial Diseases Flashcards

1
Q

What are causes of primary tubulointerstitial Nephritis

A 
Infections: acute, chronic, other
toxins: even acute Hypersensitivity interstitial nephritis
Metabolic diseases
physical factors: chronic obstruction
Neoplasms: bence jones proteins
Immunologic reactions
vascular diseases
misc
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2
Q

tubulointerstitial npehritis has was general presentations almost always

A

well inability to concentrate urine so have abnormal specific gravity and polyuria

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3
Q

what is the damage from ischemic acute tubulo injury on cell processes

A

damage to the proximal tubule brush borders

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4
Q

what will mercuric chloride poisoning look like in tubules

A

cell shave large acidophilic inclusions

totally necrotic calcification

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5
Q

what are the morphologic changes in kidneys after carbon tetrachloride poisoning

A

accumulation of neutral lipids in the cells

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6
Q

majority of UTI are due to what bacteria?

A 
enteric bacteria (gram neg)
E coli, proteus, klebsiella, enterobacter, strep faecalis, staph
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7
Q

cystitis is what and usually caued by what

A

inflammation of urinary bladder mucosa

95% bacterial

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8
Q

What is acute pyelonephritis

A

acute bacterial infection of kidney

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9
Q

what is the biggest risk with chronic pyelonephritis

A

can lead to ESRD

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10
Q

what does chronic pyelonephritis damage

A

the pelvis, calyceal system and parenchyma resulting in anatomic distortion

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11
Q

What is a predisposing anatomic defect to pyelonephritis

A

vesicoureteral reflux and assoc with intrarenal reflux

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12
Q

what are predisposing medical conditions for pyelonephritis

A

DM, pregnancy

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13
Q

what is the most common mechanism of pyelonephrtisis

A

ascending infection from lower urinary tract

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14
Q

describe cases where acute pyelonephritis might occur via hematogenous infection

A

due to septicemia or infective endocarditis

more likely if there is a ureteral obstruction, or immunocompromised

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15
Q

What is the infrarenal reflux

A

open ducts at tip of papillae
most common in upper and lower poles of kidney
papillae are flattened or concave tips at these spots

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16
Q

what are complications of acute pyelonephritis

A

papillary necrosis, pyonephrosis, perinephric abscess

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17
Q

what is bladder outlet obstruction assoc with

A

prostatic hypertrophy

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18
Q

what type of necrosis is papillary necrosis

A

coagulative
gray white yellow necrosis
tubule outlines preserved

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19
Q

What is pyonephrosis

A

when there is complete obstruction high in tract.

the pus cannot drain and fills the renal pelvis, calyces and ureter with pus

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20
Q

what is a perinephric abscess

A

pus moves through renal capsule to the perinephric tissue

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21
Q

What occurs in the healing phase of acute pyelonephritis

A

Neutrophils are replaced by macrophages, plasma cells and lymphocytes

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22
Q

What is the problem with a scar after pyelonephritis

A

associated with inflammation, fibrosis and deformation of underlying calyx and pelvis

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23
Q

what is clinical presentation of acute pyelonephritis

A

sudden onset pain at CVA, systemic evidence of infection (fever, malaise)

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24
Q

what types of nephropathies affect the calyces

A

chronic pyelonephritis and analgesic nephropathy

25
Q

on a contrast scan what is pretty indicative of vesicoureteral reflex

A

dilated ureters

26
Q

What does papillary necrosis look like in DM

A

pale gray necrosis limited to papilla

27
Q

what does analgesic nephropathy look like

A

red brown necrotic papilla sloughed into Calyx

28
Q

Xanthogranulmatous pyelonephritis is assoc with wat bacteria

A

proteus sp

29
Q

What types of drugs can cause acute drug induced interstitial nephritis

A

Sulfonamides, synthetic penicillins (methicillin, ampicillin) rifampin, diuretics(thiazides), NSAIDs
misc (allopurinol, cimetidine

30
Q

what are the clinical features of acute drug induced interstitial nephritis

A

fever, eosinophilia, interstitial renal parenchymal infiltrates, usually 15 days after exposure

31
Q

What is the pathogenesis behind drug induced acute interstitial nephritis

A

immune most likely
many have elevated IgE and IgE containing plasma cells and basophils in the lesions
making it Type I HS
some have granulomatous so type IV HS

32
Q

what are morphologicsigns of analgesic nephropathy

A

chronic tubulointerstitial nephritis and renal papillary necrosis(occurs 1st)

33
Q

What is the mech that phenacetin & aspirin mixtures cause papillary necrosis

A

depletes cell of glutathione and generates ROS

aspiring then inhibits vasodilation so susceptible to ischemia

34
Q

How do you differentiate papillary necrosis in DM compared to analgesic nephropathy

A

papillary in analgesic are at different states

DM caused necrosis the papillae are all at the same stage

35
Q

describe clinical course of analgesic nephropathy

A 
more common in women
can't concentrate urine, can lead to renal tubular acidosis, renal stones
HA anemia, GI symptoms, HTN
UTI complications! often
gross hematuria if papillae sloughed off
36
Q

Why do COX2 inhibitors still affect kidney but not GI symptoms

A

because COX2 works in kidneys

37
Q

What does Xanthogranulomatous pyelonephrtisi look like morphologically

A

foamy macrophages and plasma cells
lymphocytes and PMNs
yellowish orange nodules
looks like RCC

38
Q

How would a child present with reflux nephro[athy

A

HTN
polyuria and nocturia
asymmetrically contracted kidneys with coarse scars, blunting, deformation of calyces

39
Q

What do the kidneys scars look like if b/l chronic pyelonephritis

A

asymmetric

40
Q

What are the 3 types of nephropathy assoc with hyperuricemic disorder

A

acute uric acid nephropathy
chronic urate nephropathy
nephrolithiasis

41
Q

what is acute uric acid nephropathy and what patients is it common in

A

uric acid crystal precipitate in renal tubules (mainly collecting ducts) causing obstruction leading to renal failure
common in leukemia, lymphoma and assoc with chemotherapy

42
Q

What is chronic urate nephropathy

A

gouty. monosodium urate crystals in distal tubules and collecting ducts deposit (needle like crystals)
urates induce tophus of foreign body giant cells

43
Q

describe occurences of uric acid stones

A 
5-10% americans
80% unilateral
men more than women
hereditary predispositions
onset 20-30 y/o
44
Q

what are worse small or large kidney stones

A

small because can enter ureter and cause spasms and extreme pain

45
Q

What is nephrocalcinosis sometimes caused by

A

hyperCa, hyper PTH, multiple myeloma, vitamin D intoxication, metastatic cancer, excess Ca intake(milk alkali syndrome”

46
Q

Ca oxalate and phosphate are in what percentage of stones

A

70%

47
Q

where are Ca deposits in the tubules

A

in the mitochondria, cytoplasm and BM

48
Q

What are the predisposing conditions to Ca oxalate and phosphate stones

A 
idiopathi hypercalciuria 50%
no known abnormality 15-20%
hyperuricosuria 20%
hypercalciuria and hyper Ca 10%
hyperoxaluria, enteric, primary (the rest %)
49
Q

what is the composition of the second most common types of kidney stones

A

magnesium ammonium phosphate

50
Q

what is the most common cause of acute phosphate nephropathy

A

patients consuming high doses of oral phosphate solutions for colonoscopy prep

51
Q

what is the clinical course of acute phosphate nephropathy

A

dehydration, precipitate Ca phosphate leading to renal insufficiency after several weeks

52
Q

What can cause Myeloma kidney, or light chain cast nephropathy

A 
non renal malignancie
hypercaemia, hyper uricemia
amyloidosis
multiple myeloma
chemotherapy or irradiation
53
Q

What do bence jones proteins do in kdineys

A

combine with urinary glycoprotein Tamm Horsfall protein in acidic conditions which form large distinct casts that obstruct lumen

54
Q

Amyloidosis is deopsition of what light chain in kdiney

A

gamma

55
Q

what do bence jones tubular casts look like

A

pink or blue amorphous masses that are concentrically laminated and fractured
soemtimes surrounded by giant cells from phagocytes

56
Q

what percentage of multiple myeloma patients with myeloma kidneys progress to overt renal insufficiency

A

50%

57
Q

what is the overall clinical course of myeloma kidneys

A

chronic renal fialure is slowly progressive

acute renal failure will present with oliguria, dehydration hyper Ca, acute infection

58
Q

What percentage of multiple myeloma patients have bence jones proteins

A

70%

59
Q

What are signs of cholemic nephrosis

A

tubular bile casts that are yellow green-pink with increased serum bilirubin

Year2 Renal (20 decks)

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