Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CPR III > Renal Pathology 4: Tubular Disease (Dobson) > Flashcards

Renal Pathology 4: Tubular Disease (Dobson) Flashcards

1
Q

Two major processes that lead to AKI

A
  1. ischemic or toxic tubular injury
  2. inflammation of the tubules and interstitium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Acute Tubular Injury (ATI)

A

most common cause of AKI; damage to tubular epithelial cells and acutely diminished renal function; 50% occur in hospitalized patients reversible process; can lead to death if untreated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Ischemic ATI

A

due to decreased or interrupted blood flow (trauma, sepsis, shock)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Nephrotoxic ATI

A

may be caused by endogenous agents (gentamycin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

The two critical events of ATI

A
  1. tubular injury
  2. persistent and severe disturbances in blood flow
    leads to decreased urine output and decreased GFR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Initiation phase of ATI

A

last about 36 hours, dominate by inciting medical, surgical obstetric event; ONLY indication of renal involvement is slight decline in urine output and rise in BUN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Maintenance phase of ATI

A

oliguric crisis; sustained decreases in urine output between 40 and 400 mL/day (oliguria), salt and water overload, rise in BUN, hyperkalemia, metabolic acidosis, and other manifestations of uremia; can overcome with tx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Recovery phase of ATI

A

steady increase in urine volume that may reach 3 L/day; tubules are still damaged (large amounts of water, Na+ and K+ are lost to urine) HYPOkalmeia NOT hyperkalemia becomes clinical problem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

The 3 phases of ATI

A
  1. Initiation phase: 36 hrs, slight decline in urine output
  2. Maintenance phase: oliguric crisis; HYPERkalemia
  3. Recovery phase: increase in urine output; HYPOkalemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How are tubulointerstitial disorders distinguished clinically from glomerular diseases?

A
  1. Absence of nephritic and nephrotic syndrome
  2. Presence of defects in tubular function, evidence of polyuria or nocturia, salt wasting; diminished ability to excrete acids (metabolic acidosis); isolated defects in tubular reabsorption and secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pyelonephritis

A

inflammation of affecting tubules, interstitium, and renal pelvis. Two forms: acute and chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Acute Pyelonephritis

A

suppurative inflammation involving kidneys; generally caused by bacterial infection and associated with UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Chronic Pyelonephritis

A

more complex; bacterial infections play dominant role but other factors (VUR/obstruction) predispose to repeat episodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do the infectious organisms make it to the kidneys in Pyelonephritis?

A

hematogenous infection (Staphylococcus or E. coli) renal a. to kidneys OR UTI (E. coli) bacteria enters bladder, goes passed the vesicoureteral junction, then the VUR into the intrarenal reflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Clinical presentation of pyelonephritis

A

CVA tenderness
Systemic features (fever, elevated WBC)
Dysuria, frequency, urgency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Associations to pyelonephritis?

A

Urinary tract obstruction
Instrumentation
VUR
Pregnancy
Gender and age
Preexisting renal lesions
Diabetes
Immunodefiency

17
Q

How can uncomplicated E. coli cystitis be treated?

A

Single dose of Fosfomycin or 3 day course of TMP/SMZ or nitrofurantoin

18
Q

Viral pathogen that can cause pyelonephritis?

A

Polyomavirus; kidney allografts (renal transplants); nuclear enlargement and intranuclear inclusions visible by LM in tubular epithelial cells

19
Q

What are 3 complications of pyelonephritis?

A
  1. Papillary necrosis
  2. Pyonephrosis
  3. Perinephric abscess
20
Q

Papillary necrosis

A

mainly bilaterally; mainly diabetics, sickle cell disease, and those in urinary tract obstruction; pyramids have gray-white to yellow necrosis (coagulative) with preservation of the tubules.

21
Q

Pyonephrosis

A

total or almost complete obstruction in the urinary tract; suppurative exudate is unable to drain and fills the renal pelvis, calyces, and ureter with pus

22
Q

Perinephric abscess

A

extension of suppurative inflammation through the renal capsule into the perinephric tissue

23
Q

Why is Pelvocalyceal damage is an important diagnostic clue?

A

Because ONLY chronic pyelonephritis and analgesic nephropathy affects the renal calyces

24
Q

Uncomplicated UTI caused by Proteus mirabilis treatment?

A

3 day course of TMP/SMZ or an oral fluoroquinolones (ciprofloxacin); complicated UTI antibiotics for 10 to 21 days

25
Q

Toxins and drugs can injure kidneys is what 3 ways?

A
  1. trigger an interstitial reaction, exemplified by the acute hypersensitivity nephritis induced drugs such as methicillin
  2. cause ATI
  3. cause subclinical but cumulative injury to tubules (may be unrecognized until the renal damage is irreversible)
26
Q

Clinical presentation of drug-induced interstitial nephritis

A

fever, eosinophilia (transient), rash and renal abnormalities. a rise in Cr and AKI with oliguria develops in 50% of pts. Treatment: stop offending drugs

27
Q

Urate nephropathy

A

pts with hyperuricemic disorders (gout); acute - uric acid crystals in renal tubules; chronic - gouty nephropathy

28
Q

Autosomal Dominant Tubulointerstitial Kidney Disease (ADTKD)

A

formerly known as medullary cystic kidney disease; pathogenic mechanism are unknown; distinctive mutations: MUC1, UMOD, REN, HNF1B

29
Q

Distinctive mutations in Autosomal Dominant Tubulointerstitial Kidney Disease (ADTKD)? (4)

A
  1. MUC1 - mucin 1
  2. UMOD - uromodulin
  3. REN - preprorenin
  4. HNF1B - hepatocyte nuclear factor 1B
30
Q

Muliple myeloma

A

causes overt renal insufficiency; Bence-Jones proteinuria and nephropathy, amyloidosis of AL, light chain deposition disease, hypercalcemia and hyperuricemia

31
Q

Uromodulin

A

AKA Tamm-Horsfall Protein (THP); multifunctional protein in kidneys critical for modulating urinary and systemic homestasis

32
Q

Hepatorenal syndrome

A

form of renal failure occurring individuals with liver failure in whom there is no intrinsic morphologic or functional cause of kidney dysfxn

33
Q

Morphology of Ischemic ATI

A

focal tubular epithelial cell necrosis and BM eruption with large skip areas of unaffected tubule

34
Q

Morphology of Nephrotoxic ATI

A

focal nonspecific necrosis especially at the straight portion of the proximal tubule and the thick ascending limb

35
Q

Dirty Brown Granular cast

A

AKA renal failure cells are diagnostic for ATN

36
Q

Mycobacterium

A

can cause caseating granulomatous inflammation in the urinary tract.

CPR III (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions