Pathology Ch. 15: Tubular Diseases

Front 1

Most common cause of acute renal failure

Back 1

ATN

Front 2

Characterized by renal tubular epithelial cell destruction due to? Is this reversible?

Back 2

ATN:
Ischemia
Hypoxia due to shock, sepsis, circulatory collapse
Nephrotoxic:
Gentamycin, Cephalosporins, Mercury, lead, ethylene glycol...
It is reversible

Front 3

Pt presents with oliguria, hyperkalemia, myglobinuria, and flank pn, following extensive training for ironman?

Back 3

Nephrotoxic ATN:
Rhabdomyolysis

Front 4

ATN causes what response from the tubuloglomerular feedback system?

Back 4

Vasoconstriction of arterioles:
Renin-angiotensin
Endothelin
Decreased: NO and PGI2

Front 5

Presents as patchy tubular necrosis of the PCT, straight tubule segments, and the TAL. What does the recovery phase show?

Back 5

Ischemic ATN:
Recovery shows increased nuclei and mitotic figures with hyperchromatic cells.

Front 6

Necrotic epithelial cells cause what to occur in ATN

Back 6

Tubular obstruction do to granular casts. This leads to a still greater decrease in GFR(Increase in intratubular pressure), back leak of tubular cells(Destruction of epithelial cell barrier), and altered glomerular ultrafiltration.

Front 7

How does ischemia lead to problems in active membrane transport?

Back 7

ATP deletion stops the pumps, and causes hyperkalemia and reduced urine output. Also leads to hypernatremia

Front 8

What phase of ATN especially causes hyperkalemia, renal failure, and diminished urine production?

Back 8

Maintenance, during the recovery phase, the opposite may occur.

Front 9

A loss in polarity of the epithelial cells leads to what in ATN?

Back 9

Increase in Na delivery to the macula densa, and an increase in arteriolar constriction, decreasing the GFR even more.

Front 10

Earliest lesion of ATN

Back 10

The earliest changes in the proximal tubular cells are apical blebs and loss of the brush border membrane followed by a loss of polarity and integrity of the tight junctions. This loss of epithelial cell barrier can result in the above-mentioned back leak of filtrate

Front 11

Nephrotoxic ATN shows what tubular damage

Back 11

Only PCT

Front 12

Dysuria and increased frequency of urination? What if it also caused flank pn and fever?

Back 12

UTI
Pyelonephritis

Front 13

Why is UTI more common in women?

Back 13

Shorter urethra
hormonal changes affecting bacterial mucosal adherence

Front 14

Most common cause of pyelonephritis

Back 14

Ascending infection from the bladder

Front 15

Hematogenous pyelonephritis is due to?

Back 15

Sepsis or infective endocarditis due to S. aureus

Front 16

How does vesicouretal reflux influence pyelonephritis?

Back 16

Increases infection, usually due to a faulty intravesicular portion of the ureter, that allows urine to flow retrogradely.

Front 17

Marked by patchy, suppurative inflammation, tubular necrosis, and intratubular neutrophilic casts.

Back 17

Acute pyelo

Front 18

Tubulointerstitial inflammation that causes discrete, corticomedullary scars overlying dilated, blunted, and deformed calyces. Forms?

Back 18

CPN:
Obstructive- Causes multiple recurrences and is due to enteric bacteria.
Reflux:
Infection superimposed on vesicouretal reflux and intrarenal reflux

Front 19

Most common cause of CPN

Back 19

reflux nephropathy:
Infection superimposed on vesicouretal reflux and intrarenal reflux

Front 20

Uncommon form of CPN associated with gram- infections. Presence of foamy macrophages and yellow-orange nodules that clinically mimic renal cell carcinoma

Back 20

xanthogranulomatous pyelo

Front 21

In acute drug induced interstitial nephritis, what do the drugs act as? What happens?

Back 21

Act as haptens which bind to cellular components of the tubules, and cause the drugs to become immunogenic and secrete IgE and T cell mediated immune reactions.

Front 22

Acute drug-induced interstitial nephritis is caused by what type of rxn

Back 22

Hypersensitivity:
IgE(type 1)
T cell mediated(type 4)

Front 23

Characterized by chronic tubulointerstitial nephritis with papillary necrosis. Primary defect? cause?

Back 23

Analgesic abuse nephropathy:
Papillary necrosis is primary with tubulointerstitial nephritis secondary.
Phenacetin-aspirin-acetominophen mixtures.

Front 24

Chronic use of what may lead to analgesic nephropathy? Primary lesion?
Increased incidence of?

Back 24

Phenactin mixtures
Papillary necrosis
Transitional cell carcinoma of the renal pelvis

Front 25

Causes an increased risk of transitional cell carcinoma of the renal pelvis

Back 25

analgesic nephropathy

Front 26

Acute renal failure do to uric acid deposition is more likely in pts with? chronic renal failure?

Back 26

Hematolymphoid malignancies undergoing chemo
Gout

Front 27

Exposure to what may cause increased incidence of gout and chronic renal failure

Back 27

lead

Front 28

Combine with tubular glycoprotein to form large distinct tubular casts that obstruct the tubular lumen and induce a peritubular inflammatory rxn. Occurs in what condition?

Back 28

Bent jones proteins:
light chains
Causes proteinuria and and cast nephropathy
Multiple Meyloma...chronic renal failure

Front 29

What symtpoms of renal failure are present in multiple myeloma

Back 29

Hyperuricemia and hypercalcemia

Front 30

Deposition of light chains that can cause glomerulonephritis or tubulointerstitial nephritis

Back 30

light chain disease of multiple myeloma...proteinuria, hypercalcemia, hyperuricemia.

Front 31

Renal failure due to multiple myeloma is often due to?

Back 31

hypercalcemia...may also be due to bent-jones protein deposits, light chain deposits, hyperuricemia.

Front 32

Pathology of larger arteries in essential hypertension or diabetes mellitus

Back 32

fibroelastic thickening of the intima and media.

Front 33

Term used to describe renal changes associated with sclerosis of renal arterioles and small arteries. Characterized by?

Back 33

Benign nephrosclerosis:
Narrowing of arteriolar lumens due to wall thickening and hyalinization.

Front 34

Injury with fibrinoid necrosis of the vessel walls of the kidney by severe hypertension, thrombosis, and arteritis. Morphology? What hormones increased?

Back 34

Malignant accelerated nephrosclerosis
Fibrinoid necrosis of arterioles, onion-skinning, and necrotizing glomerulonephritis.
Increase in renin, aldosterone, angiotensin

Front 35

ἱμάτιον, τό

Back 35

clothing; coat

Front 36

Diffuse ischemic atrophy of nephrons with diffuse granular surfaces due to scarring and contraction of glomeruli

Back 36

Benign nephrosclerosis...small kidneys

Front 37

Dilation of the renal pelvis and calyces associated with progressive atrophy of the kidney following urinary outflow obstruction

Back 37

hydronephrosis

Front 38

Renal infarcts often occur in association with?

Back 38

MI or AFib

Front 39

Does hydronephrosis occur in acute or chronic settings?

Back 39

Chronic settings of partial or intermittent obstruction, where the GFR is not reduced. During acute, complete blockade, the GFR is reduced and dilation cannot occur.

Front 40

Stones associated with proteus infection

Back 40

Struvite or triple phosphate:
Contain Mg, ammonium,phosphate

Front 41

Staghorn stones occur in what setting

Back 41

Proteus infection:
Urea splitting bacteria to ammonia.
Causes struvite stones of mg, ammonium, and phosphate.

Front 42

Most renal calculi are what type

Back 42

Calcium...and due to idiopathic hypercalcemia.

Front 43

May play a role in renal stone formation

Back 43

loss of inhibitors of crystal formation.

Front 44

Cause of classic HUS

Back 44

Occurs after GI or flulike prodrome:
Verotcytotoxin-producing E Coli
Causes endothelial lysis, reduced NO.
Leads to thrombotic microangiopathies:
endothelial damage, platelet aggreagation, coagulation, and thromboses, hemolytic anemia, and renal failure.

Front 45

Endothelial injury, intravascular platelet aggregation and caogulation with thromboses, hemolytic anemia, and renal failure

Back 45

Thrmobotic microangiopathies:
Classic HUS

Front 46

HUS overlaps with?

Back 46

Idiopathic TTP