Topic 74-80: vascular, ATN, tumors Flashcards

1
Q

What are three vascular diseases of the kidney?

A
  • benign nephrosclerosis (arterionephrosclerosis): associated with benign hypertension
  • malignant nephrosclerosis: associated with malignant hypertension (BP > 200/120 mmHg)
  • thrombotic microangiopathies: widespread thrombosis in microcirculation
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2
Q

Benign nephrosclerosis is associated with what morphology?

A
  • hyaline arteriolosclerosis
  • diffuse granular kidney
  • symmetrically atrophic
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3
Q

malignant nephrosclerosis is associated with what morphology?

A
  • fibrinoid necrosis
  • hyperplastic arteriolosclerosis
  • (possibly) pinpoint petechial hemorrhage, “flea-bitten” appearance
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4
Q

Thrombotic angiopathies are what types of conditions?

A
  • Hemolytic uremic syndrome (HUS) - toxins acting on endothelial cells
  • thrombotic thrombocytopenic purpura (TTP) - vWF cleavage defect. cannot cleave vWF precursors -> extremely large vWF that increases platelet adherence and aggregation
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5
Q

Diabetic nephropathy is characterized by two conditions:

These conditions are are associated with 3 lesions:

A

Characterized generally by nephrotic syndrome and diffuse glomerulonephritis

  1. Glomerular lesions: BM thickening, Mesangial sclerosis, Kimmelstiel-Wilson
  2. Renal vascular lesions, especially arteriolosclerosis (uniquely to DM: efferent arterioles are sclerotic)
  3. Pyelonephritis, including necrotizing papillitis
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6
Q

Glomerular lesions are what 3 things specifically with diabetic nephropathy?

A
  • Glomerular BM thickening: thicker and porous
  • Diffuse mesangial sclerosis: very common, mesangial cell proliferation
  • Nodular glomerulosclerosis: PAS positive ball-like deposits in periphery of glomerulus (Kimmelstiel-Wilson lesion)
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7
Q

Diabetic Nodular sclerosis is associated with ball like deposits called? How common are they?

A
  • Kimmelstiel-wilson lesions

- not very common, only 15-30%

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8
Q

What type of pyelonephritis is more common in diabetics?

A

-necrotizing papillitis is more prevalent in diabetics

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9
Q

acute tubular necrosis is what? which parts of the tubule are affected? what are the three types of ATN?

A

ANT is damage to the tubular epithelial cells due to ischemia or toxins.

-the prox straight and thick ascending are the most affected

  • Ischemic ATN
  • nephrotoxic ATN
  • pigment ATN
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10
Q

ischemic ATN is due to what? what is the morphology/prognosis?

A
  • ischemia due to shock

- fragmentation of the BM occurs, thus there is a worse prognosis

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11
Q

Nephrotoxic ATN is due to what? prognosis?

A
  • direct toxicity due to drugs such as aminoglycosides, heavy metals
  • no BM fragmentation thus better prognosis
  • only in proximal tubules!!
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12
Q

pigment ATN is due to what? prognosis?

A
  • hemoglobin (hemolysis) or myoglobin (crush syndrome, rhabdomyolysis) will cause pigment cast to form in the tubules that obstructs flow, causing plasma leaking into the interstitium and eventually increasing pressure so much that it causes tubular collapse

–damage of BM=bad prognosis

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13
Q

Tubulointerstitial nephritis is what? what is the most common TIN infections? what are the specific types you should remember?

A
  • an infection that involves the renal tubules and interstitium. the glomeruli are spared or only affected later
  • usually caused by bacterial infections or interstitial inflam caused by drugs, physical injury, viruses, autoimmune, or metabolic disorders
  • acute and chronic pyelonephritis
  • acute drug-induced interstitial nephritis
  • analgesic abuse nephritis
  • urolithiasis
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14
Q

What are the two types of chronic pyelonephritis?

A
  • chronic obstructive - due to recurrent infections
  • chronic reflux - most common due to the congenital vesicoureteral reflux! ureter doesn’t meet bladder at an angle and thus the urine goes back when voiding the bladder
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15
Q

acute drug induced interstitial nephritis and analgesic abuse nephritis are different how?

A
  • analgesic abuse nephritis is due to people who consume large quantities of painkillers or aspirin
  • drug induced nephritis is a hypersensitivity rxn 1 or 4 to different types of drugs. symptoms occur about 2 weeks after administration and it’s because the drugs act as heptanes that bind the tubules and cause the hypersens rxn
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16
Q

what are two types of renal obstruction

A

renal stones and hydronephros

17
Q

renal stones: how do they form and where? what are the consequences? what are the 4 types?

A

urolithiasis can form at any level of the urinary collection system but most arrive in the kidney. they for due to an increased concentration of the stones constituents in the urine leading to supersaturation –> precipitation
-consequences are pyelonephritis and hydronephrosis

  • calcium stones
  • Mg- ammonium phosphate stones (staghorn calculi)
  • uric acid stones
  • cystine stones
18
Q

hydronephrosis is what?

A

literally “water inside the kidney”—refers to distension and dilation of the renal pelvis and calyces, usually caused by urinary retention due to obstruction of the free flow of urine from the kidney

leads to atrophy

19
Q

What are the two types of benign renal cancer?

A

papillary adenoma and fibroma

20
Q

What are the three types of renal carcinomas? what cell do they derive from? who are they more likely to appear in?

A

all are derived from the renal tubular epithelium

-men are twice as likely and pts with PKD due to dialysis have a 30x chance inc of kidney cancer

  • Clear cell carcinoma
  • papillary renal cell carcinoma
  • chromophobe renal carcinoma
21
Q

clear cell carcinoma is how common? occurs with what mutations or conditions?

A
  • 70-80%!

- majority are sporatic but they can occur in assocatiion with von Hippel-lindau disease (VHL)

22
Q

papillary renal cell carcinoma is how common? how do they appear? occurs with what mutations or conditions?

A
  • 10-15%
  • frequently appear multifocal and bilateral!
  • causative gene is the MET proto-oncogene on chrom 7 (tyrosine kinase receptor for hepatocyte growth factor). gene duplications or trisomy 7 will def cause cancer
23
Q

chromophobe renal carcinoma is how common? occurs with what mutations or conditions?

A
  • 5%
  • appear due to loss of entire chromosomes (can be 1,2,6,10,13,17,21)
  • good prognosis
24
Q

what are the typical symptoms of renal carcinoma?

A

symptoms vary

  • painless hematuria
  • palpable abdominal mass
  • dull flank pain
25
Q

renal cell carcinoma metastasis go where typically?

A

vertebra, lung, bone, liver, brain

26
Q

wilms tumor: how common is it? what is the cell origin? what gene mutations are common? what is the prognosis?

A
  • third most common organ cancer in children under 10 years
  • WT1 and WT2 are both tumor suppressor genes that are lost with tumor formation

the tumor originates from a variety of tissue components (all mesodermal) but there are two main forms

  • epithelial cell -mimics tubules and glomerular structures
  • stromal cell - mixed stroma with fibroblasts

generally the prognosis is excellent with treatment

27
Q

tumors of the bladder and ureter are important because? what are some predisposing factors? upon biopsy, what do they look for and why?

A

-bladder cancer is a more frequent cause of death than kidney cancer! and even a small lesion in the ureter can cause more serious problems that a large mass (due to obstruction)

  • sex (men are 3x more likely)
  • beta-naphthylamine (in cigarette smoke, 50X increased risk)
  • cigarettes
  • genetics via chrom 9 mutations

-depth of invasion is something very significant in bladder cancer biopsy analysis due to the increased risk of recurrence and worse prognosis

28
Q

what are the 3 types of bladder tumors?

A
  • benign papilloma - frond like structure
  • urothelial carcinoma - flat to papillary in shape, low to high grade, respectively
  • in-situ stage of bladder cancer

think: Big Papa trump Urinates In the Situation room

29
Q

What is the clinical course of acute tubular injury? (3 stages)

A
  1. Initiation: first 36 hours. Slight oliguria, BUN increase
  2. Maintenance: 2-6 days. Dramatic drop in urine output. Develops uremia, acidosis, fluid overload, etc. Needs good hospital care to survive.
  3. Recovery: Steady increase in urine volume, polyuria may develop. Plugs disappear from tubular system, epithelium regenerates. Still has risk of electrolyte imbalances and infection, and many still die in this phase.