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Nephrology > Infection, stones, tumors > Flashcards

Infection, stones, tumors Flashcards

1
Q

What benign renal tumors do we need to know?

A

Renal Papillary Adenoma, Angiomyolipoma, oncocytoma

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2
Q

What are the renal cell carcinoma variants we are supposed to know about?

A

Clear cell carcinoma, papillary carcinoma, chromophobe carcinoma, urothelial tumors of the calyces and pelves

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3
Q

What are renal papillary adenoma tumors?

A

Well circumscribed nodules within the cortex
*22% of people have them at autopsy so they don’t interfere with much though they are often surgically removed as “early cancers”

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4
Q

What is an angiomyolipoma?

A

tumor of messels, smooth muscle and fat. somewhat common in patients with tuberous sclerosis

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5
Q

What is an oncocytoma?

A

tumor of eosinophilic epithelial cells (not eosinophils) containing numerous mitochondria
*makes up about 10% of all renal neoplasms so it’s fairly common

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6
Q

What is the incidence of clear cell carcinoma?

A

Most common type - 80%ish of renal cell cancers, male to female ratio of 3:1

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7
Q

What are the clinical manifestations of clear cell carcinoma?

A

Hematuria

  • renal mass may be incidental finding on a different imaging study
  • arises in the renal cortex, has a propensity to invade the renal vein and can extend into the inferior vena cava up to the heart
  • regional lymph nodes may be enlarged. hematogenous spread to lungs may occur
  • metastatic disease often as multiple nodules in the lungs
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8
Q

What does clear cell carcinoma look like radiographically?

A

ball like mass of renal cortex, with the tumor less enhanced than normal parenchyma

  • engorged, tumor-filled renal vein with extension to inferior vena cava
  • evidence of metastatic disease
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9
Q

What are the pathological characteristics of clear cell carcinoma?

A
  • Gross = often as a single tumor (multifocal and bilateral in VHL), spherical, yellowish gray mass, variegated appearance, focal hemorrhage, 20% are cystic
  • Histology = three cell types, clear, granular and spindle. most tumors are composed of clear cells, granular cells or a mixture.
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10
Q

What is the gene you should think of when you see sporadic clear cell carcinoma?

A

VHL or Von Hippel Lindau tumor suppressor gene
*ubiquitin ligase complex, one of the targets being HIF-1 or hypoxia inducible factor. without degradation that leads to angiogenesis and cell growth

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11
Q

What is the treatment of choice for clear cell carcinoma?

A

nephrectomy traditionally, but more and more partial nephrectomy to preserve all the function possible

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12
Q

What is the pathological appearance of papillary carcinoma?

A

remember this is a subtype of RCC - also is considered “chromophilic”

Gross - unlike clear cell RCCs, papillary carcinomas are frequently multifocal
Histology - papillary growth pattern

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13
Q

What cancer should you think of in the kidney associated with trisomies?

A

Papillary carcinoma

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14
Q

What’s up with Chromophobe Renal Carcinoma?

A

Looks like cells with prominent cell membranes and pale eosinophilic cytoplasm, usually with a halo around the nucleus. Looks a lot like oncocytoma

  • characterized genetically by extreme hypodiploidy and chromosome loss
  • thought to come from intercalated cells
  • pretty good prognosis comparatively
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15
Q

What’s up with a collecting duct carcinoma?

A

nests of malignant cells enmeshed within a prominent fibrotic stroma, typically a medullary location

  • no distinct genetic pattern
  • poor prognosis because of aggressive behavoir
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16
Q

What are considered the hereditary neoplasms?

A

VHL syndrome (hemagioblastomas of cerebellum and retina, renal cysts and bilateral renal cell carcinomas, clear cell tumors)

  • familial clear cell carcinoma, confined to kidney but with problems with VHL gene or a related gene
  • hereditary papillary carcinoma (autosomal dominant, multiple bilateral tumors with papillary histology)
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17
Q

What are the risk factors for transitional cell neoplasms

A
  • pretty common urinary tract neoplasm, more male than female
  • urban environment
  • smoking
  • acrylamide exposure
  • Schistosoma haematobium infection
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18
Q

What are the clinical manifestations of transitional cell carcinomas?

A

90% of the tumors that arise from the urinary tract so it’s pretty common

  • hematuria (episodic, gross or microscopic), irrative bladder like dysuria, increased urgency and frequency
  • metastasis to lungs bone and liver
  • can be cause of obstruction
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19
Q

What is the pathological appearance of a transitional cell carcinoma?

A

Gross = purely papillary to nodular or flat. invasive or noninvasive
*lesions appear as red, elevated excrescences

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20
Q

What are the therapies for transitional cell carcinomas?

A

BCG vaccine to kill it with T cells, electrocautery, surgery

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21
Q

What organs can be affected in a Urinary Tract Infection?

A

Urethra, bladder, ureter, kidney

  • lower = cystitis
  • upper = pyelonephritis
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22
Q

What are the two routes by which a Urinary tract infection might arise?

A

Hematogenous (rare)
*hematogenous spread could be from septicemia or infective endocarditis. More likely in presence of ureteral obstruction, debilitation or immunosuppressive therapy.

Ascending (common, but they need to have adherence factors or pili or something to get up there)

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23
Q

What kinds of infectious organisms are more likely to cause hematogenous UTI?

A

Non-enteric organisms: staphylococci, fungi, viruses

24
Q

What is the most common cause of UTI?

A

Enteric bacteria: Fecal flora like E coli (most common)

*could also be proteus, klebsiella, enterobacter

25
Q

What are teh uro-pathogenic attributes of organisms that cause UTI?

A
  • Bacterial adhesion - adhesive omelcules on Pili/fimbria
  • O antigens - marking some more resistant strains than others
  • endotoxin (decreases ureteric peristalsis)
26
Q

What are the four categories of ‘lowered host defenses’ that predispose someone to a UTI?

A
  • mechanical (hydrokinetic) = bladder emptying and urine flow and ureteric peristalsis,
  • Chemical (urine) = prostatic secretions, urine osmolality, pH, ammonia, blood group antigens (P1 or P2)
  • immunological = IgA and complement

*celluar = PMNs, shedding urothelial cells (bacteria can be engulfed by urothelial cells)

27
Q

What’s up with vesicoureteral reflux?

A
  • predisoposes a patient to ascending UTI
  • no valve at ureterovesicle junction (bladder)
  • functional valve from oblique ureter entrance is lost when it comes straight perpendicular into the bladder
  • allows for retrograde flow into the ureter
28
Q

What can cause “secondary” vesicoureteral reflux?

A
  • Neurogenic bladder (paraplegia, spina bifida)

* bladder atony

29
Q

What are the three grades for vesicoureteral orifices?

A 
1 = normal
2= sadium orifice
3 = golf hole orifice
30
Q

What might radiographic evidence of vesicoureteral reflux be?

A

Retrograde pyelogram showing way more flow and dilatation in one ureter over another. Essentially looks like hydronephrosis

31
Q

If VUR were to continue unaltered, what might eventually happen in the kidney

A

typical coarse scars of chronic pyelonephritis due to VUR (vesicoureteral reflux)
*usually polar location and associated with underlying blunted calyces at the poles

32
Q

what are the 6 classes of urinary tract obstruction?

A
  • Intrinsic
  • stricture
  • urethral valves
  • extrinsic compression
  • functional
  • idiopathic
33
Q

What might cause intrinsic obstruction?

A

Exophytic (tumors), calculi (stones), sloughed necrotic papillae, blood clots

34
Q

How do obstruction and infection go hand-in-hand?

A

Obstruction: interferes with clearance of infection, predisposes to infection, allows for recurrence and results in chronic pyelonephritis and direct tissue injury with chronic infection

35
Q

What are the different stone compositions we talked about?

A
  • Radio-opaque = calcium oxalate and phosphate (70%)
  • Semiopaque = magnesium ammonium phosphate (15-20%)
  • not usually radioopaque = uric acid, cystine
36
Q

What factors pre-dispose somebody to stones?

A

Hypercalcemia, increased uric acid, low pH, decreased volume, bacterial infections (proteus and struvite/staghorn calculi because of urea being converted to ammonia and alkalemic urine leading to ppt)

37
Q

Where might stones get lodged?

A

Tubules, calices, pelvis, UB

38
Q

with really bad stones causing obstruction, what are the eventual consequences?

A

obstruction consequences = hydronephrosis, hydroureter, infection, chronic obstructive pyelonephritis, renal failure, hypertension

39
Q

What are the symptoms associated with acute pyelonephritis?

A

fever, malaise, nausea, vomiting, abdominal pain

40
Q

What are the symptoms associated with pyronephrosis?

A

(pernephric abcess)

rigors, loin pain, scoliosis, loin swelling, weight loss, night sweats

41
Q

What are the symptoms associated with lower urinary tract infection (cystitis)

A

dysuria, frequency, hematuria, cloudy offensive urine, nocturia, suprapubic pain, strangury, urgency

42
Q

what might cause papillary necrosis?

A

Diabetes mellitus (almost all papillae, same stage), analgesic nephropathy, sickle cell disease (rarely), obstruction

43
Q

what are the principal disease-causing organisms in pyelonephritis?

A

The principal causative organisms in acute pyelonephritis are the enteric gram-negative rods. Escherichia coli is by far the most common one. Other important organisms are Proteus, Klebsiella, Enterobacter, and Pseudomonas; these usually are associated with recurrent infections, especially in persons who undergo urinary tract manipulations or have congenital or acquired anomalies of the lower urinary tract (see later). Staphylococci and Streptococcus faecalis also may cause pyelonephritis, but they are uncommon pathogens in this setting.

44
Q

What causes renal agenesis/aplasia?

A
  • cause = failure of metanephric diverticululm to develop or its early degeneration
  • bilateral will kill the fetus
  • more often left side only, the other side hypertrophies to compensate
45
Q

What is renal dysplasia?

A

abnormal metanephric tissue differentiation of the kidney tissue with cysts and heterotopic tissues such as cartilage due to pleuripotent potential of renal anlage

46
Q

What do you worry about in horseshoe kidney?

A
  • inappropriate fusion of the kidney anlage and they don’t rise fully
  • increased incidence of nephroliathisis
47
Q

What is the most common renal mass?

A

Simple acquired cyst

*usually asymptomatic

48
Q

On a radiograph you may see radioopaque medullary lesions and that might suggest what?

A

Medullary sponge kidney

  • common finding in people with recurrent kidney stones
  • normal sized kidneys but enlarged and pale renal pyramid(s)
  • 1/2 contain calcifications which is what is radioopaque
49
Q

What is ARCD?

A

Acquired renal cystic disease

  • in patients with ESRD that are on dialysis, this is pretty common
  • can be asymptomatic but can cause pain, hematuria, renal colic or palpable mass
  • worry about renal cell carcinoma developing from it
50
Q

What is Autosomal dominant polycystic kidney disease?

A

PKD1 (majority) or PKD2 mutations (polycystin proteins)

  • near 100% penetrance with large cysts
  • kidneys bilaterally enlarged up to 40cm because of multiple variably sized renal cysts distributed relatively uniformly through the medulla and cortex containing clear to hemorrhagic fluid
  • hepatic cysts are also common here
51
Q

What are the common accompanying abnormalities in autosomal dominant polycystic kidney disease?

A

Hepatic cysts, mitral valve prolapse, diverticulosis, cerebral aneurysms, pancreatic cysts

52
Q

When and how does autosomal dominant polycystic kidney disease present?

A

usually in 4th decade with chronic flank pain or intermittent hematuria

  • HTN and CKD in 5th decade
  • 1/2 progress to ESRD
53
Q

What disease is due to a mutation in PKHD1?

A

autosomal recessive polycystic kidney disease

  • enlarged kidneys bilaterally (same as autosomal dominant) but they still look like kidneys
  • a whole bunch of smaller cysts mostly
  • cysts are dilated collecting tubules here
54
Q

In autosomal recessive PKD what organ besides the kidney is affected

A

Liver is ALWAYS affected in this condition. It is fibrotic (congenital hepatic fibrosis = CHF)

55
Q

How does autosomal recessive PKD present?

A

Hypertension early in life and diminished urine concentrating ability, renal insufficiency.

  • can cause growth retardation
  • can (rare-ish) require transplant
56
Q

What is NMCD?

A

NMCD = nephronophthisis-medullary cystic kidney disease complex

  • most common cause of ESRD within the first 2 decades of life
  • related to MCKD or medullary cystic kidney disease which is an autosomal dominant form
  • bilateral small kidneys show cortical atrophy with a thickened, pitted, granular, capsular surface
  • sperical cysts in corticomedullary junction
  • 1/4 cases don’t even have cysts

Nephrology (14 decks)

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