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Pathology Block C > Kidneys II - Tubulointerstitials, Congenital, Adenomas > Flashcards

Kidneys II - Tubulointerstitials, Congenital, Adenomas Flashcards

1
Q

What are the characteristics of acute tubular necrosis?

A

multiple etiologies

major cause of acute renal failure

usu reversible (can reconstruct itself to restore functionality- labile)

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2
Q

What are the two broad categories of acute tubular necrosis?

A

ischemic (patchy necrosis)

nephrotoxic (segmental e.g. proximal convoluted tubule)

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3
Q

Where do we see ischemic ATN?

A

scattered along length of PCT and loops of Henle - does NOT afect just one focal segment

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4
Q

What are some causes for ischemic ATN?

A

1) thrombus/embolus
2) massive exsanguinations (GSW, trauma, etc)
3) hypovolemia/shock (blood being shunted away from kidneys)

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5
Q

Where do we see nephrotoxic ATN?

A

tend to be segmental, or more focal, particularly within PCT

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6
Q

What is unique to nephrotoxic ATN?

A

sudden onset, which results in coagulative necrosis of renal tubular epithelium

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7
Q

What is this?

A

ATN

key feature here: cortical pallow (esp. in ischemic subtype)

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8
Q

What is this?

A

cortical necrosis of ATN- see fibrosis, scarring, and contraction

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9
Q

What’s the treatment for ATN?

A

vasopressin - to get BP back up and regulate fluid volumes,

make sure kidneys are perfused

dialysis

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10
Q

What are some characteristics of acute pyelonephritis?

A

bacterial infection (usu gram neg)

ascending or hematogenous routes

associated with urine stasis, obstruction, retrograde flow (cystitis to pyelonephritis)

patchy interstitial suppurative inflammation (microabscesses)

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11
Q

Does acute pyelonephritis start as cortical disease?

A

NO! as the disease worsens, it can affect the cortex

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12
Q

What is this?

A

pyuria = pus in urine (so PMNs and RBCs)

NOT pathognomonic

seen in acute pyelonephritis

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13
Q

What is another key feature of acute pyelonephritis?

A

WBC casts - indicative of inflammation/infection

can potentially have 2 different kinds - renal tubular or epithelial casts

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14
Q

Where do the WBC cast originate from?

A

ONLY renal tubule​- so this means it CANNOT be a lower UTI (has to originate in the kidney itself)

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15
Q

What is shown here?

A

acute pyelonephritis - enlarged and swollen

microabscesses: tiny yellow dots scattered throughout cortex and medulla (CLASSIC sign of inflammation)

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16
Q

What happens to microabscesses?

A

will become dropout areas - no longer able to perform renal functions

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17
Q

What is the cause of the flank pain seen in acute pyelonephritis?

A

stretching of the kidney’s capsule due to the enlargement of the organ secondary to inflammatory mediators and infiltrates

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18
Q

What is shown here?

A

chronic pyelonephritis

note the grossly scarred kidneys

19
Q

What causes chronic pyelonephritis?

A

interstitial fibrosis and atrophy of tubules due to multiple bouts of acute pyelonephritis

20
Q

toxins or drugs inducing acute immunologic (hypersensitivity) reaction in the interstitium - resulting in interstitial inflammation with predominantly _?_

progression?

A

Interstitial nephritis

eosinophils ; papillary necrosis

21
Q

What is seen histologically in TID - Interstitial Necrosis?

A
  1. tubules separated (should be back-to-back)
  2. interstitium full of inflammatory cells
  3. normal glomeruli
  4. eosinophils!
22
Q

What is this?

A

papillary necrosis - yellowish-softening coagulative necrosis of medullary pyramid papillae

23
Q

What is this?

What happens when sloughs off?

A

papillary necrosis!

  1. get acute onset of anuria (bc the tubes get blocked)- lose ability to concentrate urine
24
Q

What are the causes of papillary necrosis?

A
  1. acute pyelonephritis
  2. interstitial nephritis
  3. diabetic nephropathy
  4. sickle cell disease
  5. nephrotoxity drugs
25
Q

How does hypertension lead to renovascular disease (RVD)?

A

hypertension-> medial thickening-> progress decrease in perfusion of renal cortex -> atrophy

*long standing hypertension is leading cause for dialysis and transplant*

26
Q

How does benign nephrosclerosis lead to RVD?

A

renal ischemia leads to symmetrically atrophic kidneys -> glomerular dropout -> tubular dropout

*chronically can be fatal becomes too shrunken over time*

27
Q

How does accelerated nephrosclerosis (malignant HTN) lead to RVD?

A

Medical emergency!

sudden rise of BP to extreme high levels -> intimal endothelial changes and necrosis of endothelium of small arterioles

28
Q
  1. characterized by thrombosis in capillaries and arterioles throughout body
  2. hemolytic anemia
  3. thrombocytopenia
  4. renal failure (cause of mortality)
A

microangipathy

29
Q

How is renal artery stenosis associated with RVD?

A

(acquired through atherosclerosis or congenital)

Goldblatt kidney: constriction of renal a. causes ischemia and release of renin leading to HTN

30
Q

How is thrombotic microangiopathic disorders related to RVD?

A

group of disorders caused by activation of intrinsic coagulation system

fibrin threads produced -> clogged kidney’s microvasculature -> ischemia

“wire through cheese” analogy: fibrin threads slice RBCs -> hemolytic anemia

31
Q

Microangiopathies are NOT diagnosed with?

A

kidney biopsy!

32
Q

Examples of microangiopathy?

A

HUS, thrombotic thrombocytopenia purpura, eclampsia and pre-eclampsia, lupus, malignant hypertension, DIC, etc

33
Q

What’s the underlying pathophysiology of microangiopathy?

A

triggering of coagulation system => thromboses in microvasculature throughout body -> fibrin monomers -> hemolyic anemia

34
Q

How do infarcts present in RVD?

A

embolic, peripheral, wedge shaped, coagulation necrosis, clinically silent (bc significant functional reserve)

35
Q

What is this?

How is it manifested at birth? over time? palpable? mode inheritance?

A

adult polycystic disease

  1. present but functional
  2. cysts grow and put pressure causing pressure atrophy of underlying renal tissue -> renal insufficiency and possible microhematuria
  3. yes!
  4. autosomal dominany
36
Q

What is this?

fetus manifestation? cause? mode of inheritance?

A

Cystic Dysplasia (pediatrics)

  1. survive in utero bc of mom’s kidneys but lethal after birth
  2. failure of normal embryonic development
  3. autosomal recessive
37
Q

What is this?

cause? clincal presentation? diagnosis? treatment?

A

Simple Cyst

  1. acquired
  2. usu asymptomatic bc kidneys normal function; rupturing= fluid into retroperitoneal space causing pain and irritation that subsides over couple of days
  3. US or CT
  4. rarely need treatment
38
Q
  1. most often derived from renal tubular epithelial cells that fail to produce tubules or nephron structures
  2. localized lesion under 1.5cm

metastasis?

A

adenoma

as grow >2cm -> rates of metastatic disease rise (so debate if truly benign or renal cell CA in waiting)

39
Q
  1. relatively common
  2. usu eccentric (at one pole or the other- NOT homogenous); usu. slow growing
  3. solid, large, lobulated mass beneath capsule; zones of necrosis and hemorrhage;
  4. distant metasis (usu. silent for a while bc located in retroperitonium, but signs from metastic lesions); where invades?
A

renal cell carcinoma (aka clear cell tumor or hypernephroma)

predilection to invade renal vein -> sending tumor emboli into circulation -> metastases

40
Q
  1. pediatric tumor of embryonal appearing tissue (one of the most common intra-abdominal peds tumors)-> large globular masses; more homogenous
  2. often genetics (not always)
  3. uni/bilateral

treat? histo?

A

Wilm’s tumor

can be curative with chemo

histo: spindle cell and mesenchymal-like cell (blue cell)

41
Q
  1. papillary tumors composed of ?
  2. cauliflower appearance that can occur anywhere there is __ epithelium
A

translational cell carcinoma

transitional - duh

42
Q

Obstruction of kidneys results in? Two types?

A

anuria

  1. acute = dull flank pain
  2. extrinsic = intermittent-> colicky pain
43
Q
  1. buildup of fluid in kidneys as result of obstruction of renal outflow tract
  2. dilation of ureters ABOVE the obstruction - cysts? how to determine?
  3. one possible cause?
A

hydronephrosis

  1. not cystic! the dilations are CONNECTED (cysts don’t connect)
  2. congenital urethral outlet stricture
44
Q
  1. pyelonephritis (define) + hydronephrosis
  2. can cause bladder distension if obstruction is in lower urinary tract leading to ? because?
  3. an ascending infection (cystitis -> ureritis -> pyelonephritis)
  4. grossly dilated ureters; destroyed kidneys filled with purulent, granular exudate and necrotic debris
A

Pyonephritis

  1. Kidney infection

2. vesicoureteral reflux: reflux of fluid from bladder back into ureters and renal pelvis bc ureterovesicl junction failed to remain closed

Pathology Block C (7 decks)

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