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Unit 7 > Tubulointerstitial infections > Flashcards

Tubulointerstitial infections Flashcards

1
Q

what are the diseases affecting the tubules/interstitium?

A
  • acute tubular necrosis

- tubulointersititial nephritis

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2
Q

what is the causative reason for Acute tubular necrosis

A
  • ischemia-vascular diseases, shock, trauma, acute pancreatitis
  • toxic injury-drugs, radiocontrast, DIC, urinary obstruction
  • toxins such as NSAIDs, antibiotics, contrast, rhabdomyolysis, hemolysis
  • prolonged pre-renal azotemia
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3
Q

what happens in acute tubular necrosis

A
  • combination of degeneration and regeneration
  • destruction of tubular epithelial cells
  • acute diminution/loss of function
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4
Q

what are some of the presentations of acute tubular necrosis?

A
  • usually oligoanuric
  • can be polyuric
  • granular casts, sloughed tubular epithelial cells
  • swollen pale kidney
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5
Q

what are some etiologies of tubulointerstitial nephritis

A

UTI and toxins

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6
Q

the extracellular cells in tubulointerstitial nephritis is located where?

A

inflammation in the interstitial area and also in the tubules
-you will see neutrophils, eosinophils, and it is usually associated with hypersensitivity reaction

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7
Q

what are the manifestations of acute pyelonephritis?

A
  • it is usually due to a bladder infection that climbs up. an ascending infection and infects the kidney. Reflux of urine
  • it is also associated with UTI and bacteria
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8
Q

what are the manifestations of chronic pyelonephritis?

A

-it is usually because of a combination of bacteria, reflux and obstruction

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9
Q

what type of bacteria is pyelonephritis associated with?

A

85% gram negative bacilli-bowel flora- e.coli, enterobacter, klebsiella, and proteus

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10
Q

the most common type of pyelonephritis is usually

A
  • ascending rather than hematogenous
  • ascending infection results from a combination of urinary bladder infection vesicoureteral reflux, and intrarenal reflux
  • hematogenous infection results from bacteremic spread.
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11
Q

what are some of the predisposing factors for polynephritis?

A
  • Structural abnormalities- e.g fistulas
  • obstruction- e.g tumors, clculi
  • kidney damage
  • residual urine that remains in the bladder even though you feel you have completely voided.
  • Getting a uti because you haven’t completely voided the bladder
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12
Q

urine is normally sterile so how does infection occur?

A

urine normally sterile but bacteria colonize distal urethra/introitus and carriage from urethra to the bladder–> bacteria grow in bladder–>reflux infection ascends

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13
Q

what do you see in an acute pyelonephritis?

A
  • patchy interstitial suppurative inflammation
  • intratubular neutrophils
  • tubular necrosis
  • wedge shaped areas of suppuration
  • abscess formation and inflammation
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14
Q

what are some complications of acute pyelonephritis?

A
  • papillary necrosis: mainly in diabetics, or with urinary tract obstruction
  • papillae slough off and can cause obstruction
  • pyonephrosis (entire kidney itself is a dilated bag of pus
  • perinephric abscess (huge abscess around the whole kidney)
  • heals by scarring (u shaped-inflammation, v shaped-vascular)
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15
Q

what are the only two diseases that affect the calyces?

A

-acute pyelonephritis that progresses to chronic pyelo and analgesic (ex: tylenol) nephropathy are the only two diseases that affect the calyces

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16
Q

what are the two patterns of chronic pyelonephritis?

A
  • reflux nephropathy

- chronic obstructive pyelonephritis

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17
Q

the typical coarse scars of chronic pyelonephritis associated with vesicoureteral reflux is

A

usually polar and are associated with underlying blunted calyces

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18
Q

in chronic pyelonephritis you will see

A
  • scars
  • fibrosis
  • blunted calyces
  • decrease/shrinkage in size
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19
Q

what are some of the manifestations of benign nephrosclerosis?

A
  • disease of the blood vessel
  • you get sclerosis of arterioles and small arteries
  • it is associated w/hypertension, diabetes
  • medial and intimal thickening w/hyaline deposition
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20
Q

what are the chances of benign nephrosclerosis progressing to renal failure

A

rarely progresses to renal failure

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21
Q

what would you expect to see of the kidney in a benign nephrosclerosis?

A

fine, leathery granularity of surface

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22
Q

what manifestations do you see in malignant hypertension and accelerated nephrosclerosis?

A
  • develops de novo or be superimposed on previous benign hypertension
  • 1-5% of hypertensive patients
  • you see it in younger, male, and african-american
23
Q

what do you see in the kidney of a patient with malignant nephrosclerosis?

A
  • irregular surfaces with small hemorrhages
  • fibrinoid necrosis of arterioles (vessel wall destroyed)
  • onion skinning (hyperplastic arteriolitis)(narrowed lumen)
  • fibrinoid necrosis of afferent arteriole (PAS stain)
24
Q

what is the name of the condition when you see little clots in the glomeruli?

A

thrombotic microangiopathies

25
Q

what is the classic cause of thrombotic microangiopathy

A

Hemolytic uremic sydrome (bloody diarrhea due to infection w/ verotoxin releasing bacteria

26
Q

what are the characteristics of thrombotic microangiopathies?

A
  • endothelial injury and activation w/ intravascular thrombosis
  • platelet aggregation
  • subsequent vascular obstruction and vasoconstriction
  • distal ischemia
  • you’ll see fibrin thrombi
27
Q

the classiv thrombotic microangiopathy picture is associated with

A
  • verotoxin producing E. Coli
  • type 0157:H7
  • hamburgers
  • GI or flu-like syndrome precedes
  • GI bleeding, oliguria, hematuria
  • usually recover w/short term dialysis, but may sustain permanent damage
28
Q

often after surgery or instrumentation dislodges you can get?

A
  • atheromatous plaques from aorta/renal artery can embolize.

- emboli usually have no consequences unless numerous or underlying poor renal function

29
Q

diffuse cortical necrosis involves what and it often happens after

A
  • necrosis of your entire cortex after something traumatic/catastrophic where you don’t perfuse kidney
  • often after ob emergency such as abruption(placental)
  • ischemic changes, thrombi
30
Q

what are the most common form of bilateral renal cortical necrosis and least common

A
  • most common is obstetric complications: 1. abruptio placenta 2. septic abortion(infected miscarriage)
  • least common is non-obstetric: 1. Shock/DIC 2. Acute pancreatitis 3. Aortic dissection 4. Hyperacute allograft rejection
31
Q

what is the etiology of renal cortical necrosis

A
  • intense vasospasm of the small vessels
  • if this vasospasm is brief and vascular flow is reestablished, acute tubular necrosis results
  • more prolonged vasospasm can cause necrosis and thrombosis of the distal arterioles and glomeruli, and RCN ensues
32
Q

renal infarcts common site is? and why?

A 
the kidneys. 
because :
-it receives 25% of cardiac output
-thees minimal collateral circulation
-it is usually embolic
-from heart after MI most common
-after vegetative endocarditis, aortic aneurysm thromboemboli, aortic atherosclerosus
33
Q

contrast the renal infarct with pyelonephritis

A

it has a wedge shaped infarct and is v-shaped scar which is different from the U-shape in pyelonephritis

34
Q

what are the congenital anomalies associated with the kidneys

A
  • agenesis
  • hypoplasia
  • ectopic kidneys
  • horseshoe kidney
  • ureteral duplication
35
Q

cystic renal dysplasia is associated with

A

obstruction and usually a pediatric condition

36
Q

polycystic kidney disease has two types but both types are present

A

autosomal dominant- shows up in adulthood
autosomal recessive- shows up in childhood
both are present at birth

37
Q

acquired cystic diseases of the kidney usually happen during___ and have a chance of

A

dialysis and have a 7% chance of becoming renal cell carcinoma

38
Q

what are the characteristics of cystic renal dysplasia?

A
  • it is the most common cystic disease in children; no inheritance pattern
  • abnormality of metanephric differentiation
  • cartilage, undifferentiated mesenchym that cuffs around the immature collecting tubules
  • abnormal lobar organization
39
Q

what is cystic renal dysplasia often associated with

A

obstruction and it be be unilateral or bilateral

40
Q

what is the clinical presentation of a patient with autosomal dominant polycystic kidney disease? What can it present with?

A
  • presents in adults 40-60 years of age
  • large multicystic kidneys
  • Liver cysts
  • berry aneurysms
  • cardiac valve abnormalities(mitral valve prolapse)
  • hematuria, flank pain, UTI, stones, HBP
  • leads to chronic renal failure
41
Q

what are the common dialysis patients with ADPCKD

A

-patients with diabetes and hypertension

42
Q

what is the mutation associated with ADPCKD?

A

defect in PKD1 gene that codes for protein polycystin 1 and PKD2 that codes for polycystin 2

43
Q

what is the difference between autosomal dominant and autosomal recessive?

A

instead of the large cysts seen in AD in AR you have smaller cysts and dilated channels at right angles to the cortical surface. also in AD you have liver cysts

44
Q

what are the characteristics of ARPCKD

A
  • huge cystic kidneys at birth
  • congenital hepatic fibrosis (ductal plates of the liver)
  • defect in gene PKHD1 that codes for protein fibrocystin
45
Q

what is ARPCKD associated with?

A

Giant abdomen that compresses the chest; this is associated with potter sequence and oligohydramnios. Don’t die from uremia or renal failure(takes a while to develop); die from hypoplastic lungs

46
Q

what are the characteristics of medullary sponge kidney?

A
  • less severe and very rare
  • seen in adults, unknown etiology
  • associated with calcifications in dilated ducts, hematuria, infection, urinary calculi
  • renal function usually normal
  • recurrent hematuria, UTI, and renal stones
47
Q

nephronopthisis characteristics and what does it result in

A
  • childhood onset
  • has medullary cysts at corticomedullary junction
  • small kidneys
  • cortical tubulointerstitial damage w/ eventual renal insufficiency
  • medullary cysts with cortical tubulointerstitial disease later on that results in renal insufficiency
48
Q

dialysis associated cysts are probably due to

A
  • obstruction of tubules by fibrosis or oxalate crystals
  • they may be asymptomatic
  • risk of RCC 7%
  • cortical and medullary cysts, 0.5-2 cm
49
Q

simple cysts are

A

idiopathic; they mean nothing; can be seen in normal kidney

50
Q

what are the characteristics of obstructive uropathy?

A
  • increases risks of infection and stones
  • renal damage-hydronephrosis if unrelieved
  • can be sudden or over time
  • can have obstruction at any level of the tract
  • can have severe pain or no pain
51
Q

what are the causes of obstructive uropathy?

A
  • intrinsic or extrinsic
  • anomalies such as posterior urethral valves, urethral strictures, upj obstruction
  • urinary calculi
  • BPH (hyperplstic prostate) very common cause of incomplete obstruction
  • carcinoma of pelvic organs: prostate, bladder, cervix, uterus, retroperitoneal lymphoma
52
Q

what are some associations with obstructive uropathy?

A
  • inflammation of prostate, ureter, urethra
  • sloughed paillae or clots
  • normal pregnancy
  • uterine prolapse/cystocele
  • functional disorders-neurogenic (spinal cord damage, diabetic nnephropathy)
53
Q

Urolithiasis (renal calculi, stones) presents with

A
  • frequent
  • Males more than female
  • age peak 20-30 but can happen in any age
  • may be associated with hereditary metabolic disorders such as gout, cystinuria, primary hyperoxaluria
54
Q

what are the benign tumors of the kidney

A
  • renal papillary adenoma
  • renal hamartoma
  • angiomyolipoma
  • oncocytoma

Unit 7 (13 decks)

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