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CPR Exam 2 > Chapter 20.2 Tubular and Intersitial Diseases > Flashcards

Chapter 20.2 Tubular and Intersitial Diseases Flashcards

1
Q

What is acute renal failure (acute kidney injury)??

A
  • Acute decline in renal function (fall in GFR => ↑ BUN/Cr) that is usually reversible.
  • Often, results in tubular necrosis.
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2
Q

What are 2 major causes of acute renal failure (acute kidney injury)?

Which is the most common?

A
  1. Acute Tubular Injury/Necrosis
  2. Poor renal perfusion
  • Most common: acute tubular injury
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3
Q

Most common cause of acute renal failure/AKI is

A

Acute tubular injury

-due to acute pyelonephritis

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4
Q
  • What is damaged in acute tubular injury?
A

tubular epithelial cells

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5
Q

What are the 2 most common causes of Acute Tubular Injury?

A
  1. Ischemia of the kidneys
  2. Dierct toxic injury of tubules (drugs/ toxins)
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6
Q

How does the pattern of tubular damage in the proximal tubule and ascending loop of henle seen in acute tubular injury differ between ischemic and toxic sources?

A
  • Both see same amount of casts in same areas, but different patterns of necrosis.
  • Ischemia causes
    • Patchy necrosis in proximal tubule and TALoH
  • ​Toxic injury causes
    • Continuous necrosis in proximal tubule & patchy necrosis in TALoH
  • Both have epithelial casts that occlude the lumen of TALoH (patchy) => DCT => CD
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7
Q

Why are tubular epithelial cells particularly vulnerable to ischemia?

A
  • Increased SA for reabsorption
  • High NRG requirements because many mT and need O2
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8
Q
  • How will toxicities affect proximal epithelial cells?
A
  • widespread injury, resuling in swelling and vacuolization
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9
Q

In ATI, what occurs to necrotic tubular epithelial cells over time?

Leads to?

A

Die, slough into lumen of tubule and obstruct urine flow, forming granular casts in tubules that are muddy brown.

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10
Q

Can proximal epithelial cells regenerate?

A

Yes, as long as the BM is intact

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11
Q

How does ischemic ATI cause necrosis of tubular cells?

A
  • Ischemic ATI => vasoconstriction => decrease in GFR and necrosis of tubular cells
    • Vasoconstriction occurs due to loss of tubular cell polarity: Na/K ATPase moves from BL side => luminal side of tubular epithelial cell, pumping Na+ into the urine
    • Na+ is sensed by macula densa => triggering vasoconstriction
    • => decrease in GFR
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12
Q

Ischemic ATI occurs in what situations?

A
  • hypovolemia, cardiogenic shock, massive bleeding
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13
Q
  • Toxic ATI is caused by what drugs and toxins?
A
  1. Ethylene glycol (anti-freeze)
  2. Aminoglycosides
  3. Heavy medals (e.g. lead)
  4. Myoglobinuria from crush injury
  5. Radiocontrast dye
  6. Urate (e.g. tumor lysis syndrome
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14
Q

What are the 3 stages of the clinical course of AKI/ARF due to ATI and major electrolyte/lab findings in each stage?

Which stage is marked by an increases susceptibility to infection?

A
  1. Initiation– Injury occurs
    • Lasts 36 hrs, we see a slight decline or pee (oliguria)
  2. Maintenance
  • Low urine output with uremic features
  • Hyperkalemia
  • Metabolic acidosis
  1. Recovery (depends on duration and nature)
  • High urine output: polyuria (3L/day) => loss of water, Na, K, hypokalemia
    • muscle problems
  • Susceptible to infection
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15
Q

What is the prognosis of ATI dependent on?

How likely are these pts to survive?

A
  • Magnitude and duration of injury
  • Recovery is typical, some may need dialysis
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16
Q

What is Tubulointerstitial Nephritis

A
  • Group of renal diseases that cause inflammation of renal tubules and interstitium.
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17
Q
  • Tubulointerstitial Nephritis is generally characterized by what 2 things?
A
  1. Insidious onset
  2. Azotemia due to decrease GFR, making it difficult to concentrate urine (polyuria and nocturia)
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18
Q
  • What are the clinical hallmarks of Tubulointerstitial Nephritis that distinguish it from Glomerular diseases?
A
  1. NO nephritic or nephrotic syndrome
  2. Defects in tubular function –> defect in concentrating urine = polyuria and nocturia
  3. Salt wasting
  4. Dimished ability to excrete acids (metabolic acidosis)
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19
Q
  • What causes tubulointestinal nephritis?
A
  • 1. Infection: acute, chronic, other
  • 2. Toxins
  • 3. Metabolic diseases
  • 4. Physical factors (chronic obstruction)
  • 5. Neoplasm (Bence-Jones proteins)
  • 6. Immunological reactions
  • 7. Vasular diseases
  • 8. Other
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20
Q

Acute Tubulointerstitial Nephritis has what 3 characteristics?

A
  • Rapid onset
  • Characterized by
    • interstitial edema
    • leukocytic infiltration in tubules and interstitium
    • Tubular injury
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21
Q

Chronic Tubulointerstitial Nephritis has what 3 characteristics?

A
  1. mononuclear leukocytes
  2. interstitial fibrosis
  3. lots of tubular atrophy
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22
Q
  • How can we tell if it is acute/chronic tubulointerstitial nephritis ?
A
  • If edema is present with eosinophils/neutrophils => acute
  • If fibrosis and tubular atrophy => chronic
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23
Q

What is a UTI?

A
  • An infection anywhere along the urinary tract from urethra => renal cortex.
  • Can cause tubulointestitial nephritis
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24
Q

85% of UTIs due to what?

A

Enteric bacteria (e.coli)

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25
Q

What are the most common causes of UTIs?

A

Gram (-) rods:

  • 1. E.coli
    1. Proteus
    1. Klebsiella or Enterobacter
    1. streptococcus faecalis
    1. staph
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26
Q

What bacteria causes UTIs and produces urease, which can cause struvite kidney stones?

A

Proetus mirabilis

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27
Q

Most UTIs are ________ infections.

A

Ascending, from a lower urinary tract infection: urethra => cystitis => pyelonephritis

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28
Q
  • _______________ is what allows bacteria to gain access to ureters, while stasis makes it easier
A
  • Vesicoureteral Reflux (VUR)
    • ​Congenital: malformed or incompetent valve
    • Acquired: atony of bladder
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29
Q

What is the Intrarenal Reflux?

A
  • Infected bladder urine d/t VUR => renal pelvis and deep into the renal parenchyma through via tips of the papillae
30
Q
  • Absence of VUR cause what types of infections?
A

Lower UTI (cystitis and urethertiis): infection remains localized to the bladder.

31
Q

What is the source of infections in UTI and who are they more common in?

A
  • Patients fecal flora
  • Women bc shorter urethra
32
Q

What type of UTIs do we most commonly see in clinical practice?

A

Lower UTIs

33
Q

What is cystitis?

What is it mainly due to?

A
  • Infection and inflammation of the LUT (bladder mucosa)
  • 95% due to bacteria (e.coli)
34
Q

Cystitis is a lower urinary tract that causes what symptoms?

A

pain with urination (dysuria), frequency/urgency, suprapubic pain, NO systemic symptoms (no fevers, chills, sweats)

35
Q

Pyelonephritis is an infection of the

A

kidneys; tubules, interstitium, renal pelvis

36
Q

Most common cause of clinical pyelonephritis arises from what?

A

Ascending infection from the bladder

37
Q

Who is most likely to get pyelonephritis?

A

Patient with a predisposing anatomic defect: VUR and intrarenal reflex

38
Q

What are 2 of the common predisposing medical conditions for Pyelonephritis?

A

1. DM

2. Pregnant people

39
Q

What is the vesicoureteral reflux?

A
  1. Incompetence of the vesicoureteral valve that causes urine to reflux from bladder => ureter => kidney
40
Q

How can vesicoureteal reflux be acquired in both children and adults?

A
  • Children –> congenital defect (most common) when the intravesical protion of the ureter does not NTR the bladder oliquelym causing a backflow of piss.
  • Adults –> obstruction, often due to prostatic hypertrophy
41
Q

Vesicoureteral reflux can be diagnosed via a ______________.

  • What will we see
A
  • Voiding cystourethrogram.
    • Hydronephrosis (Dilated ureter)
42
Q

Although ascending infection is the most common route of bacteria entering the kidney, they may also do so hematogenously, which is most often occurs in what clinical setting?

A

Sepsis

43
Q

Acute Pyelonephritis is acute bacterial infection of the kidney that is almost always the result of

A

[ascending cystitis infection + predisposing anatomic defect [vesicoureteral junction or obstruction of bladder outlet].

44
Q

What is a viral pathogen causing pyelonephritis in kidney allografts often leading to the development of nephropathy/allograft failure?

A

Polyomavirus

45
Q

Drug and toxin-induced tubulointersitial nephritis is the SECOND most common cause of what?

A

AKI (acute renal failure)

46
Q

Acute pyelonephritis is most common in who?

A

Females from infancy to age 40

47
Q

What are sx of acute pyelonephritis?

A
  1. Sudden onset CVA tenderness
  2. SYSTEMIC SIGNS – fever and malaise (whereas with cystitis there are no systemic signs)
  3. WBC Casts
48
Q

Which has systemic signs: cystitis or acute pyelonephritis?

A

acute pyelonephritis

49
Q

What are the morphological hallmarks of Acute Pyelonephritis?

Is the glomerulus affected?

A
  1. Patchy interstitial suppurative inflammation
  2. Aggregates of neutrophils (WBC) in tubules
  3. Neutrophilic tubulitis
  4. Tubular necrosis
  5. Glomerulus is NOT affected
50
Q

Grossly, what does acute pyelonephritis look like?

A

multiple foci of areas of yellow-greyish-white acute inflammation (liquefactive necrosis, pus) & abscesses

51
Q

What complications are assocaited with Acute Pyelonephritis?

A
  1. Papillary Necrosis
  2. Pyonephrosis: pus accumulation in pelvis, calyx, ureter that obstructs kidney
  3. Perinephric abcess
52
Q

What is Chronic Pyelonephritis?

A

chronic tubuloiterstitial inflammation and renal scarring with of the calyces, pelvis and parenchyma.

53
Q

What are hallmarks of Chronic Pyelonephritis?

A
  1. Corticomedullary scaring with blunted/deformed calyces and flattened papilla in upper/lower poles
  2. Interstitial fibrosis and atrophy of tubules
  3. Hyaline arteriosclerosis
  4. Thyroidiization of the kidney: tubules contain eosinophil-protein materal and look like thyroid follicles
54
Q

VUR w/chronic pyelonephritis à

A

polar cortical scarring

55
Q

Xanthogranulomatous Pyelonephritis is a rare form of chronic pyelonephritis associated with ______

A

proteus

56
Q

Xanthogranulomatous pyelonephritis is a rare form of chronic pyelonephritis characterized by the accumulation of what?

Associated with what infection?

The large, yellowish orange nodules may be clinically confused with?

A
  • accumulation of foamy macrophages w/ plasma cells, lymphocytes, PMN leukocytes, giant cells
  • Proteus infection
  • Renal cell carcinoma
    *
57
Q

Chronic Pyelonephritis may develop into ?

A

FSGS => ESRD

58
Q

Papillary necrosis is a complication of acute pyelonephritis most often seen in which 4 patients/settings?

A
  • 1) Diabetics
  • 2) Analgesic Nephropathy
  • 3) Urinary tract obstruction
  • 4) Sickle Cell Disease
59
Q

What is papillary necrosis?

A
  • Coagulative necrosis of renal papillae.
  • Sloughing off of the tissue causes gross hematuria that is often painless; renal function is often NL.
60
Q

What is the M:F ratio for papillary necrosis associated with diabetes mellitus?

Time course?

How do the papillae appear and are they calcified?

A
  • F
  • 10 years
  • Pale, greyish necrosis of ONLY papilla
61
Q

What is the M:F ratio for papillary necrosis associated with Analgesic Nephropathy (NSAIDS)?

Time course of abuse?

How does the necrosis appear on the papillae, how diffuse is the necrosis and is there calcification?

A
  • F
  • 7 years
  • Red-brown necrotic papilla sloughed into calyces with frequent calcification
62
Q

Which gender has a higher incidence of papillary necrosis as a result of obstruction?

Are calcifications rare or frequent?

A
  • Males
  • Frequent
63
Q

Only what 2 entities causing renal damage affect the calyces,making pelvocalyceal damage an important diagnostic clue?

A

1) Chronic pyelonephritis

2) Analgesic nephropathy

64
Q

What is Acute (Drug-Induced) TubuloInterstitial Nephritis?

A
  • Hypersensitivity Type I and 4 reaction to a number of drugs that cause tubulitis and acute renal failure
65
Q

TUBULOINTERSTITIAL NEPHRITIS CAUSED BY DRUGS (ALLERGIC NEPHRITIS)

Why is it clinically important to recognize drug-induced acute interstitial nephritis?

A

Withdrawl of the offending drug is followd by recovery, which may take several months

66
Q

Does Acute (Drug-Induced) TubuloInterstitial Nephritis depend on the dose?

A

NO

67
Q

How do drugs cause Acute (Drug-Induced) TubuloInterstitial Nephritis?

A
  • Drugs acts as a hapten until concentrated in the tubules to be excreted in urine.
  • Then, they activate IgE and T/B/Plasma cells in the localized area
68
Q
  • What are patients with analgesic nephropathy more likely to develop?
A
  • Urothelial carcinoma of the renal pelvis
69
Q

NSAIDs have been shown to cause what 2 renal syndromes developing concurrently?

A

- Acute interstitial nephritis

- Minimal change disease

70
Q
A

CPR Exam 2 (29 decks)

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