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RCS > L11- Tubular and Interstitial Diseases > Flashcards

L11- Tubular and Interstitial Diseases Flashcards

1
Q

list some examples of tubular and interstitial kidney diseases

A
  • ATN (acute tubular necrosis)
  • tubulointerstitial nephritis
  • acute polynephritis
  • chronic polynephritis
  • papillary necrosis
  • obstructive nephropathy
  • renal stones
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2
Q

ATN is the result of irreversible injury to (1) causing cell death, aka (2), and eventually progresses to (3). The major causes are (4) and (5).

A 
(acute tubular necrosis)
1- renal tubules
2- necrois
3- ARF (acute renal failure- an intrinsic and pre-renal cause)
4- ischemia (more common)
5- toxicity
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3
Q

list the 3 major signs and symptoms of ATN

A
  • acute decline in GFR
  • oliguria / anuria
  • serum BUN and creatinine increased
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4
Q

list the possible causes of ischemic ATN

A
  • hypotension
  • vasodilatory systemic infection (septic shock)
  • hemorrhagic shock (GI bleed)
  • hypovolemic shock (vomiting, diarrhea)
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5
Q

list the possible causes of Nephrotoxic ATN

A

Exogenous: i) aminoglycosides, ii) contrast media (CT/cardiac cath)

Endogenous: i) hemoglobinuria, ii) myoglobinuria

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6
Q

Ischemic ATN- has a (diffuse/patchy) necrosis affecting (2) parts of the nephron the most

Nephrotoxic ATN- has (diffuse/patchy) necrosis affecting (4) parts the most

A

1- patchy: short segments affected
2- straight PCT, ascending LoH

3- diffuse: more extensive
4- PCT

Note- both affect DCT, particularly ascending LoH

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7
Q

describe how toxic and ischemic injury in ATN leads to oliguria/anuria and reduced GFR

A

Ischemia:

i) vasoconstriction –> dec GFR + tubular injury
ii) tubular injury –> tubular backleak, sloughed cells, interstial inflammation
iii) backleak –> dec urine output / inflammation –> dec GFR / sloughed cells => obstruction –> dec urine and dec GFR

Toxic: skips (i), direct tubular injury

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8
Q

list the 3 clinical phases of ATN

A
  • initiation phase (36 hrs)
  • maintenance phase
  • recovery phase
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9
Q

in the initiation phase of ATN there is an acute decrease in (1) and a rapid increase in (2)

A

(1st 36 hrs)
1- GFR
2- serum BUN, creatinine

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10
Q

the maintenance phase of ATN can last for (1), and there is a plateau of (2); key signs and symptoms include (3), therefore (4) may be necessary

A 
(2nd phase)
1- days - 3 wks (oliguria)
2- serum BUN, creatinine
3- uremic Sxs, fluid overload, metabolic acidosis, hyperkalemia (=> arrhythmias / death)
4- dialysis
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11
Q

in the recovery phase of ATN, (1) is restored, leading to an increase in (2) and (3) and a (rapid/gradual) decrease in (5)

A 
(3rd and final phase)
1- tubular function
2- GFR
3- urine output / volume
4- gradual
5- serum BUN, creatinine
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12
Q

list the physical exam findings for ATN Dx

A
  • hypotension
  • low urine output = oliguria/anuria
  • uremic signs: pericardial friction rub, confusion
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13
Q

list the laboratory (non-urine) findings for ATN

A
  • elevated serum BUN, creatinine
  • metabolic acidosis / low HCO3-
  • hyperkalemia
  • hyperphosphatemia
  • anemia (dec EPO - more of a chronic development)
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14
Q

list the urine findings for ATN

A
  • muddy brown granular casts
  • epithelial cell casts
  • free epithelial cells
  • mild proteinuria
  • microscopic/mild hematuria
  • no pyuria (WBCs/pus)
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15
Q

tubulointerstitial nephritis defines a group of diseases with the following changes to interstitium and glomeruli

A
  • **interstitial inflammation: edema (acute), fibrosis (chronic)
  • normal glomeruli
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16
Q

Tubular dysfunction (specifically in tubulointersitial nephritis) will have the following 4 consequences:…

A
  • impaired urinary concentration (polyuria, nocturia)
  • salt wasting (hyponatremia)
  • metabolic acidosis (dec ability to excrete acid)
  • NO significant proteinuria, hematuria
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17
Q

list the acute causes of tubulointerstitial nephritis (TIN)

A
  • drugs (71%), mainly antibiotics
  • infections (15%)
  • idiopathic (8%)
  • sarcoidosis (1%)
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18
Q

list the chronic causes of tubulointerstitial nephritis (TIN)

A
  • infection (pyelonephritis = bacterial; can also be due to viral, parasitic infections)
  • analgesic abuse (ASA, acetaminophen)
  • urate nephropathy (gout)
19
Q

list the common drugs that cause tubulointerstitial nephritis (TIN)

A

(usually acute, but ASA/acetaminophen abuse causes chronic // many are antibiotics***)

  • β-lactams (penicillins, cephalosporins)
  • sulfonamides (bactrim, furosemide, thiazide diuretics)
  • ciprofloxacin
  • rifampin
  • NSAIDs***
  • cimetidine
  • allopurinol
  • PPIs***: omeprazole, lansoprazole
20
Q

Drug induced AIN is usually due to a (1) reaction with (2) infiltrating the renal interstitium. It usually appears (3) after starting medication for the first time, or (4) upon second exposure. It will have the following signs and symptoms: (5).

A 
(acute interstitial nephritis)
1- allergic reaction
2- eosinophils, lymphocytes, macrophages
3- 2 weeks
4- 3-5 days
5- (allergic rxn Sxs) fever (27%), rash (15%), eosinophilia (23%), all three (10%) OR ARF / oliguria OR asymptomatic
21
Q

list the laboratory findings in AIN

A

(acute interstitial nephritis)
Urine: eosinophils, sterile pyuria, WBC casts, mild proteinuria

Blood: inc BUN, creatinine, eosinophils + hyperkalemia and low HCO3- (via tubular dysfunction)

22
Q

AIN diagnosis is complete via (1) and treat involves (2) and (3). The prognosis of AIN can be either (4) or (5).

A 
(acute interstitial nephritis)
1- renal biopsy
2- stop drug
3- oral steroids to aid recovery
4- complete recovery
5- incomplete (40%): persistent creatinine elevation
23
Q

in acute pyelonephritis, the affecting microbes enter the kidney through either (1) or (2) [indicate which is more common]

A

1- bloodstream: seeding from distant source, i.e. bacterial endocarditis, septicemia

2- (more common) ascending infection: from lower urinary tract (bladder, ureter)

24
Q

in acute pyelonephrits where the initial infection starts in the bladder:

  • women bacterial sources are (1)
  • men bacterial sources are (2)
A

1- bacterial colonization of introitus (vaginal opening) and distal urethra –> bladder due to short urethra and can stem from Foley’s cath. or sexual intercourse

2- entry into bladder (with bacterial colonization) due to BPH (obstruction), catheterization, urine stasis, retrograde travel up to ureters then kidneys (vesicoureteral reflux- more in chlidren)

25
Q

list the clinical manifestations of acute pyelonephritis

A
  • fever
  • dysuria
  • flank pain, costovertebral angle tenderness
  • n/v
26
Q

list the 4 complications of acute pyelonephritis

A
  • papillary necrosis
  • pyonephrosis
  • perinephric abscess
  • chronic pyelonephritis
27
Q

list the laboratory findings of acute pyelonephritis

A

Urine: pyuria, bacteria, WBC casts (neutrophils, eosinophils –> drugs)

Blood: elevated BUN, creatinine (volume depletion), elevated WBCs

28
Q

Chronic pyelonephritis is due to (1) or (2), particularly in patients with (3). There is associated (4) in the kidney and eventually it progresses to (5).

A

1- recurrent / persistent renal infection
2- chronic tubulointerstitial nephritis
3- anatomical abnormalities
4- renal scarring
5- ESRD, due to decline in renal function (needs dialysis and transplant)

29
Q

list the 2 forms of chronic pyelonephritis, indicate the more common form

A
  • chronic obstructive pyelonephritis: posterior urethral valves, kidney stones
  • (more common, children) reflux nephropathy: vesiculoureteral reflux (VUR)
30
Q

reflux pyelonephritis has a (1) onset, therefore patients present (2) and will usually have the following signs and symptoms: (3)

A

1- silent onset
2- late in course of disease
3- renal insufficiency, HTN, mild proteinuria (or significant with FSGS)

31
Q

compare the gross appearance of the 2 forms of chronic pyelonephritis

A

Obstructive: diffuse dilatation of calyces and scarring

VUR: preferential scarring and calyceal dilatation at poles

32
Q

describe the microscopic appearance of chronic pyelonephritis

A
  • tubular atrophy
  • chronic interstitial inflammation
  • cortical and medullary fibrosis
  • FSGS
33
Q

papillary necrosis is usually due to the ingestion of large quantities of (1) which will cause either (2) or (3) leading to (4)

A

1- analgesics: phenacetin, ASA, caffeine, acetaminophen, codeine
2- direct toxic effect (acetaminophen)
3- ischemic effect (ASA inhibits PG)
4- chronic tubulointerstitial nephritis

34
Q

in papillary necrosis due to chronic analgesic abuse there will be attempted excretion of (1) causing (2) and (3), which can lead to (4) or (5)

A 
1- necrotic papilla
2- gross hematuria
3- renal colic (ureter obstruction)
4- progressive renal failure
5- urothelial carcinoma (rare)
35
Q

papillary necrosis due to pyelonephritis is a (un-/common) and (benign/serious) disorder where (3) will lead to the compression of (4) resulting in (5); it is treated by (6)

A 
1/2- uncommon, serious disorder
3- interstitial inflammation
4- medullary vasculature
5- ischemia, papillary necrosis
6- IV antibiotic for underlying infection
36
Q

Obstructive uropathy is a blockage in the (1) (uni-/bi-)laterally, with the following as common causes: (3).

A

1- any level of urinary tract: urethra to renal pelvis
2- either uni-/bi-lateral
3- BPH, bladder CA, kidney stone, retroperitoneal adenopathy, papillary necrosis (sloughed papillae)

37
Q

Obstructive Uropathy causes hydronephrosis by continued filtration leading to (1) dilatation and fluid diffusing into (2). The high pressure in (1) is transmitted to (3) and leads to (4). Renal function recovers if (5) occurs, or renal failure (irreversible damage) occurs if obstruction persists for (6).

A 
1- renal pelvis and calyces (walls thin)
2- interstitium
3- CTs --> renal cortex (cortex thins)
4- renal atrophy
5- relieved fast
6- 2-3 wks
38
Q

Renal stones are usually seen in the (1) age group, affecting (men/women) most. It is caused by (3).

A

1- 20-30 y/o
2- men > women
3- idiopathic or specific disease (gout, cystinuria, hyperoxaluria)

39
Q

list the types of renal stones in order of popularity

A

1) Ca containing: Ca-oxalate (Ca-C2O4), Ca-PO4 (75%)
2) struvite (Mg/NH4-PO4, usually due to infection, can be very large and obstruct renal pelvis)
3) uric acid (5%)
4) cystine (1-2%)

40
Q

renal stone = ….

A

nephrolithiasis

41
Q

Renal stones are ‘silent’ in (1) and become symptomatic in (2). It is characterized by the following three complications: (3).

A

1- renal pelvis
2- passes into ureters
3-
i) renal colic: abrupt onset of flank pain radiating to groin intermittently –> n/v, hematuria (gross/microscopic - ulceration of urothelium)
ii) superimposed UTI: urinary stasis, trauma
iii) hydronephrosis via ureter obstruction

42
Q

renal stone treatment involves…

A
  • IV antibiotics

- urological intervention (surgery, US)

43
Q

describe methods to prevent renal stones

A

Dec urinary concentration of causing substances:

  • inc fluid intake (2 L/day)
  • low Na diet (dec urinary Ca excretion b/c Ca is reabsorbed in PCT with Na)
  • alkalinisation of urine –> inc uric acid solubility

RCS (29 decks)

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