Tubulointerstitial Disease

Question 0

Acute kidney injury comes in two varieties

Answer 0

ischemic

toxic

Question 1

two reversible diseases that dont require much attention

Answer 1

osmotioc nephrosis (hypertonic solution causes foamy, disteneded PT)
hyaline droplet change (increased protein loss causes increased protein resorption)

Question 2

Acute renal failure decribed as

Answer 2

decreased GFR
oliguria
increased BUN
increased creatinine

Question 3

mechanisms of acute renal failure

Answer 3

VC of aff arteriole–>decreased perfusion–>decreased GFR
casts obstruct the tubule (increase tubule luminal pressure, decreased glomerular transcap perfusion pressure)
tubular backleak–>accum of protein products in interstitum–>increase interstital oncotic and decrease tubular oncotic–>tubules collapse

Question 4

what kind of catsts in acute kidney injury

Answer 4

granular

Question 5

toxic AKI

Answer 5

diffusely hypereosinophilic tubules with necrosis and sloughing of epithelial cells into the lumen

Question 6

3 phases of AKI

Answer 6

initiating phase (1-2 days)
maintenance phase
recovery phase (days-weeks)

Question 7

initiating phase

Answer 7

mild decrease in urine output

Question 8

maintenance phase

Answer 8

sustained decrease in urine output
water and salt retention
increase in BUN, Cr, K, metabolic acidosis

Question 9

recovery phase

Answer 9

increase in urine output (>3 l/day) with decrease in BUN, Cr, K

Question 10

clinical manifestations of tubulointerstital disease

Answer 10

decreased urine concentration (polyuria)
decrease in Na reabsorption (salt wasting)
decrease in acid secretion (metabolic acidosis)

Question 11

2 major categories of tubulointerestital disease

Answer 11

pyelonephritis: infection

tubulo-interstital: non-infectious

Question 12

4 types of tubulo-interstital nephritis

Answer 12

drug/toxin induced
analgesic abuse
urate nephropathy
myeloma kidney

Question 13

common bugs of pyelonephritis

Answer 13

g negative bacili (e cioli, proteus, klebsiella, enterobacter)
strep fecalis, staph, fungi,

Question 14

pathogenesis if comes from blood (pyelo)

Answer 14

infecting agent enters blood through ALL regions of kidney–>gross miliary distribution of microabsecesses

*lovalized to tubules and interstitum

Question 15

pathogeneiss if ascending pylo

Answer 15

colonization of urethra–>bladder–>incompetence of vescio-ureteral orifice–>reflux–>infectious agent colonizes pailla

Question 16

microscopically with ascending puelo

Answer 16

streaking distribution

Question 17

complications of acute pyelonephritis (4)

Answer 17

papillary necrosis
pyonephrosis
perinephric abscess
scarring

Question 18

papillary necrosis is common in

Answer 18

ascending PN in DM, outflow obstruction

*usually bilateral

Question 19

pyeonephrosis

Answer 19

accumulation of pus in kidney to the point where it becomse a big abscess

Question 20

peripnephric abscess

Answer 20

when the pyonephrotic kidney bursts, releasing contents into periphery

Question 21

scarring

Answer 21

broad shaped or ushaped, more common in upper or lower poles

Question 22

chronic pyeloneprhitis cannot___because___

Answer 22

be diagnozed with LM of bx alone because we need to see deformity

Question 23

MC of chornic pyelo

Answer 23

reflux, but obstructive exists too

Question 24

most frequent cause of toxic tubulointerstital nephritis

Answer 24

synthetic penicillins/antibiotics (rifampin) diuretics (thiazides) Nsaids (phenylbutazone) cimetidine

Question 25

50% of drug tin dvelope

Answer 25

acute renal failure

Question 26

pathogenesis of drug TIN

Answer 26

delayed Ige hypersens to lypmphovytes Macrophages EOSINOPHILS

Question 27

pathology drug induced TIN

Answer 27

lymphocytes in pathces but key is eosinophils

Question 28

anaglesic abuse nephropathy is caused by

Answer 28

mass intake of phenacetin, aspirin, caffeine, acetaminophin, codeine

Question 29

how does acetominophin hurt cells

Answer 29

covalent binding and oxidation

Question 30

how does aspirin hurt cells

Answer 30

blocks PGE-->VC-->ischemia

Question 31

what kind of pathology with analgesic abuse nephro

Answer 31

papillary necrosis

Question 32

three types of urate nephropathy

Answer 32

acute uric acid chronic urate nephrolithiasis

Question 33

acute uric acid nephro

Answer 33

ppy of urate crystasls in CD-->obstruction | **common in chemo

Question 34

chronic uratenephropathy

Answer 34

patients with hyperuricemia | trophus formation- needle like crystals surrounded by giant cells

Question 35

nephrolithiasis is seen with

Answer 35

gout patietns

Question 36

patho in myeloma kidney

Answer 36

brittle (fractured) cast formation-->obstruction +/- granulomas