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Pathology Post Midterm > Module 4: Renal: Tubular and Interstitial Diseases > Flashcards

Module 4: Renal: Tubular and Interstitial Diseases Flashcards

1
Q

Before we get into the specific diseases lets talk about casts, what are they?

A

Indicates a problem in the glomerulus or tubules

  • -made of Tamm-Horsefall proteins
  • -casts take the shape of the tubules
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2
Q

What are the various types of casts?

A 
Hyaline Casts: 
--physiological: only one from dehydration or exercise 
Granular (muddy brown): 
--acute tubular necrosis (hypovolemic  shock or hypotension) 
Waxy: 
--chronic renal failure and broad based 
RBC cast: 
--nephritic syndrome 
WBC cast: 
--acute pyelonephritis (PMNs) and Allergic Interstitial Nephritis (Eosinophils) (following drugs, rash, and fever, and azotemia) 
Lipid Casts: 
--nephrotic syndrome 
WBCs in urine: 
--acute pyelonephritis or allergic interstitial nephritis or cystitis 
RBCs in urine 
--nephritic syndrome or bladder cancer 
Oval fat bodies: 
--nephrotic syndrome
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3
Q

When can you see casts in the urine below the kidneys?

A

Only if hydronephrosis is present

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4
Q

Now moving onto conditions of the tubes. What are the two major causes of acute tubular necrosis?

A

Ischemic and toxic

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5
Q

What are the predictable phases of acute renal failure?

A

Initiation Phase (36 hours)
–Acute decrease in GFR and rapid increase in serum creatinine and BUN
Maintenance Phase:
–Plateau of serum creatinine and BUN
–Lasts for days to 3 weeks (oliguria)
–Uremic symptoms, fluid overload, metabolic acidosis and hyperkalemia (requires dialysis)
Recovery Phase:
–Tubular function restored, increased GFR and increased urine volume
–gradual decrease in creatinine and BUN

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6
Q

What do you find in urine and on labwork for acute tubular necrosis?

A

Urine findings: muddy brown casts, epithelial casts, free epithelial casts, mild proteinuria, microscopic hematuria and no pyuria
Lab: Increased serum creatinine and BUN, metabolic acidosis, hyperkalemia, hyperphosphatemia and anemia (decreased EPO)

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7
Q

What is found on PE and histology for acute tubular necrosis?

A

PE: hypotension, oliguria and uremic symptoms
Histology: coagulative necrosis of the tubules

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8
Q

What are complications of acute tubular necrosis?

A

Ischemic Insult: hypotension, vasodilatory (septic shock) systemic infection, hemorrhagic shock (GI bleeding), hypovolemic shock (vomiting and diarrhea)
Nephrotoxic: Exogenous= aminoglycosies
and endogenous= hemoglobinuria and myglobinuria

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9
Q

Moving onto Tubulointerstitial Nephritis, what is the tubular dysfunction?

A
  • -Impaired urinary concentration (polyuria, and nocturia)
  • -Salt wasting (hyponatremia)
  • -Metabolic acidosis (decreased ability to excrete acid)
  • -No significant protenuia/hematuria
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10
Q

What is the etiology for tubulointerstitial Nephritis?

A
  • Acute: drugs(abx), infection, idiopathic, and sarcoidosis

- -chronic: infection (pyleonephritis), analgesic abuse, urate nephropathy

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11
Q

any random facts?

A

ssds

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12
Q

Moving onto the next tubular syndrome is acute drug induced Interstitial Nephritis. What is the etiology?

A

Penicillin (Abx), cephalosporin, NSAIDs, sulfonamides, ciprofloxacin, rifampin, cimetidine, allopurinol, and proton pump inhibitors.

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13
Q

What is the pathogenesis for acute drug inducted interstitial nephritis?

A

Allergic type reaction manifested by interstitial infiltration of eosinophils, lymphocyte and macrophages
–onset 2 weeks after first exposure or 3-5 days if 2nd exposure

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14
Q

What is the presentation for acute drug induced interstitial nephritis?

A 
Fever 
Rash 
Eosinophilia 
ARF 
Oliguria
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15
Q

What is seen on blood and urine for acute drug induced interstitial nephritis?

A

Urine: eosinophils, sterile, pyuria (without bacteria), WBC casts, proteinuria
Blood: Increased BUN and creatinine, increased eosinophils and tubular dysfunction (increased K and decreased HCO3)

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16
Q

What is the treatment for acute drug induced interstitial nephritis?

A

Stop using drug = complete recovery

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17
Q

Next topic for tubular pathology is acute pyelonephritis. What population do you see this in and why?

A

More common in females

–due to shorter urethra

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18
Q

What are the two routes for infection?

A

Due to E. coli
Ascending infection from the bladder (most common)
Descending infection via hematogenous spread (sepsis (Emboli) or infective endocarditis on the left side)

19
Q

What are the risk factors for acute pyelonephritis?

A

Ascending:

  1. Bladder: bladder stones, bladder cancer or VUR (pediatric vesicoureteral reflux)
  2. Prostate: prostate cancer or BPH
  3. Cervix: cervical cancer
  4. Urethra: Urethral Strictures: chronic gonorrhea, chronic chlamydia and chronic schistosoma hematobium
  5. Pregnancy: hydronephrosis
  6. Diabetes: autonomic neuropathy: prevents voiding of urine in the bladder due to paralyzed parasympathetics and therefore stasis of urine in the bladder = cystitis
  7. Catheters
20
Q

What is the presentation for acute pyelo?

A 
Sudden onset 
--fever 
--chills 
--flank pain 
CVA tenderness
Cystitis: dysuria, increased frequency and increased urgency
21
Q

What is seen in the urine analysis and blood for acute pyelo?

A

WBC casts: indicates kidney damage
Nitrates: organism converts nitrates to nitrites
Blood: Increased BUN and creatinine due to volume depletion

22
Q

What is seen on gross and histology for acute pyelo?

A

Gross: Swollen, red and foci of pus (yellow stuff on kidney)
Histology: tubulonterstitial disease (PMNs occlude the lumen of the tubule and therefore come out as WBC casts) — spares glomerulus (normal GFR)

23
Q

What are the three P’s to complications for acute pyelo?

A

Papillary necrosis
Pyonephrosis
Perinephric Abscess

24
Q

Patients with acute pyelo can get FSGS, how?

A

VUR:
–the angle at which the ureters go into the kidney is abnormal in these kids and therefore urine goes to the lower and upper poles so they get pyelonephritis acute which turns chronic. So therefore eventual fibrosis of the upper and lower poles. Therefore compensatory hyperfiltration that leads to FSGS.

25
Q

What are the two forms of chronic pyelonephritis?

A
  1. Chronic obstructive pyelonephritis: posterior urethral valves and kidney stones – diffuse dilatation of calcyes and scarring
  2. Reflux Nephropathy (more common):
    - -vesicoureteral reflux (VUR) – preferential scarring and calyceal dilatation to poles
    - -silent onset
    - -renal insufficiency and HTN
26
Q

What is seen on microscopy of patients with chronic pyelo?

A

Tubular atrophy
Chronic interstitial Inflammation
Fibrosis in cortex and medulla

27
Q

What is the complication of chronic Pyelo?

A

progression to FSGS

28
Q

Moving on to Papillary necrosis. What is the etiology?

A

Papillary Necrosis and Chronic Analgesic abuse: phenacetin, ASA (aspirin/NSAIDs), caffeine, acetaminophen and codeine

29
Q

What is the pathogenesis for papillary necrosis?

A

Ingestion of large quantities – papillary damage due to direct toxic effect (Acetaminophen) and ischemic effect of ASA (inhibition PG — abnormal vasoconstriction of intrarenal arteries) —chronic tubulointerstitial nephritis

30
Q

What is the presentation for papillary necrosis?

A

Intravenous Pyelogram (IVP): ring defect at the tips of minor calyces

  • -progressive renal failure
  • -gross hematuria, colicky flank pain (ureter obstruction)
31
Q

What is the pathogenesis for papillary necrosis pyelonephritis?

A

Interstitial inflammation compress medullary vasculature —- ischemia and papillary necrosis
–treat underlying infection

32
Q

Moving onto obstructive nephropathy and hydronephrosis, what is the etiology?

A

BPH, cervical, prostate or bladder cancer, kidney stone, strictures, horeshoe kideny, VUR, retroperitoneal adenopathy, papillary necrosis

33
Q

What is the pathogenesis for nephropathy and hydronephrosis?

A

Continued glomerular filtration but unable to excrete due to obstruction – dilatation of renal pelvis and calyces
-high pressure in pelvis is transmitted through collecting tubules into cortex – renal atrophy and thinning of renal cortex

34
Q

What is seen on US in patients with nephropathy/ hydronephrosis?

A

Thinning of renal cortex and dilatation of renal pelvis and calyces

35
Q

What are the three different types of hydronephrosis?

A
  1. Unilateral: asymptomatic
  2. Bilateral Incomplete: cause below the ureters so initially polyuria because effects ability of tubule to concentrate urine – develop chronic renal failure (waxy casts) and white cell casts — anuria and uremia
  3. Bilateral Complete: below the ureters — urine backs up into the blood — anuria — uremia
36
Q

What are the complications of hydronephrosis?

A

Stasis — stones and kidney infections
Chronic renal failure
Irreversible damage and renal failure if obstruction not relieved by 2-3 weeks

37
Q

Finally the last topic in tubular defects is renal stones or renal calculi, describe the gross images

A

Left Image: Nephrolithiasis (kidney stone or renal calculi) located in the PUJ (pelvicuretero junction) – site of the white arrow
Right Image: Dilation of the Calyces and pelvis and atrophy of the cortex and medulla — hydronephrosis — complication of nephrolithiasis

38
Q

What are the three main types of stones?

A
  1. Calcium Oxalate/Phosphate (75%): primary hyperparathyroidism is the most common cause of these stones (parathyroid adenoma making PTH). Oxalate is made in acidic environments and Phosphate is made in basic environments
  2. Struvite Stone (made of Mg, Ammonium and phosphate): form a staghorn calculus associated with UTIs (huge stones that fill up the entire kidney)
  3. Uric Acid Stones: associated with states of hyperuricemia in cancer patients or patients with gout due to elevated uric acid levels
  4. Cystine Stones
39
Q

What is the pathogenesis for renal stones?

A

Excessive excretion of minerals in the urine

40
Q

What is the most common site for kidney stones?

A

PUJ due to the bend in the anatomy of the ureter

41
Q

What is the presentation for renal stones?

A

Men greater than women with peak incidence 20-30 y.o

  • -silent if remain in renal pelvis
  • -symptomatic if stone passes into ureters
  • -coliky pain that radiates to the groin
  • n/v
  • -gross or microscopic hematuria
42
Q

What investigations are done for renal stones?

A

Best: US – stone and dilatation of calyces and pelvis
CT with KUB (kidney, ureter and bladder) checking urogenital tract.
–uric acid stones are radiolucent so they wont be seen
Urinalysis: WBC casts if hydronephrosis and possibly waxy if renal failure and RBCs

43
Q

What are the complications associated with kidney stones?

A
  1. Urinary stasis – infections
  2. Chronic renal failure
  3. Hydronephrosis: kidney stone is the most common cause of this, anything that obstructs the bladder or urethra can cause this
44
Q

What are some prevention advice to give to patients?

A

Increased fluid intake
Low sodium diet
Alkalization of urine (By staying hydrated)

Pathology Post Midterm (50 decks)

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