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CPR II Exam 2 > Ch 20 > Flashcards

Ch 20 Flashcards

1
Q

more hematuria**, usually sicker

  • caused by glomerular disease
  • RBC’s in urine, red cell casts on UA
  • pt presents with acute post-streptococcal glomerulonephritis
A

Nephritic syndrome

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2
Q

severe proteinuria** (>3.5 g/24 hours)

  • low molecular weight proteins in urine (highly selective)
  • hypoalbuminemia, hyperlipidemia, lipiduria
  • subepithelial deposits**
A

Nephrotic syndrome

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3
Q

rapid decline in GFR with concurrent dysregulation of electrolytes and fluid, retention of metabolic waste products

A

Acute Kidney Injury (AKI)

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4
Q

diminished GFR that is persistently less than 60ml/min for at least 3 months and/or persistent albuminuria
- Major cause of death from renal disease

A

Chronic Kidney disease

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5
Q

disorders in which the kidney is the only or predominant organ involved

A

primary glomerulonephritis

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6
Q

when the glomerulus is affected by systemic immunologic disease such as SLE, vascular disorders such as HTN or metabolic diseases

A

secondary glomerulonephritis

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7
Q

when there is no cellular inflammatory component

A

glomerulopathy

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8
Q
  • Antibody binding PLA2 receptor present in glomerular epithelial cell membrane, followed by complement activation
  • immune complex deposition along the sub-epithelium of the basement membrane
  • granular IF pattern
A

Nephrotic syndrome (membranous nephropathy)

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9
Q

simultaneous lung and kidney lesions (hematuria and hemoptysis) due to anti-GBM Ab’s that cross react with other basement membranes (especially in lung alveoli)
- linear IF pattern

A

Goodpasture syndrome

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10
Q

progressive fibrosis that leads to proteinuria and hematuria (stems from a loss of renal mass)

  • often associated with systemic HTN
  • nephrotic syndrome WITH nephritic syndrome
A

Focal Segmental Gloemrulosclerosis (FSGS)

- most common cause of nephritic syndrome in adults

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11
Q

What is the treatment for FSGS?

A

Renin-Angiotensin System inhibitors

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12
Q

fibrosis and inflammation of the tubules and interstitium (opposed to the glomerulus)
- results from either direct injury from proteinuria/cytokines, or tubules over-expressing adhesion molecules that stimulate inflammatory response

A

Tubulointerstitial Fibrosis

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13
Q

1-4 weeks after untreated infection:

  • formation of immune complex formation in situ/deposition of antibody against pyogenic exotoxin B (SpeB)
  • “hump-like” deposits in subepithelial space
  • diffuse proliferation of glomerular cells (enlarged and hypercellular) associated with influx of leukocytes
  • granular IF deposits of IgG and C3
A

Post-Streptococcal Glomerulonephritis (PSGN)

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14
Q

6-10 year old pt, with sudden/abrupt onset of malaise, fever, nausea, periorbital edema, mild-moderate HTN, oliguria, proteinuria, dysmorphic RBC casts and hematuria 1-2 weeks post-infection
- labs show elevated ASO, low serum complement levels

A

PSGN

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15
Q

What can cause Non-streptococcal acute glomerulonephritis?

A

other infections: Staph endocarditis, P. pneumonia, meningococcemia, HepB, HepC, mumps, HIV, varicalla, mononucleosis, Toxoplasmosis, Malaria

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16
Q

How does Non-strep acute glomerulonephritis differ from PSGN?

A

sometime it can produce immune deposits containing IgA rather than IgG

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17
Q

anti-GBM antibodies that cross react with pulmonary alverolar BM, anti-collagen type 4

  • antigen is alpha3 chain of collagen type 4
  • associated with HLA-DRB1
  • leads to renal failure in weeks-months if left untreated
A

Type 1 Rapidly Progressive Glomerulonephritis (RPcGN)

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18
Q

How do you treat RPcGN type 1?

A

plasmapheresis (remove Ag/Ab from circulation)

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19
Q
  • immune complex deposition with granular pattern of immune complex formation
  • cellular proliferation and crescent formation
  • NOT helped by plasmapheresis
A

Type 2 RPcGN

- must treat the underlying cause

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20
Q
  • no anti-GBM complexes or immune complexes, but associated with anti-neutrophil cytoplasmic antibodies (ANCA**)
  • idiopathic, manifestation of small-vessel vasculitis or polyangiitis (known to play a role in some vasculidities like granulomatosis with polyangiitis
A

Type 3 RPcGN

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21
Q
  • hematuria, red cell casts, proteinuria approaching nephrotic ranges
  • variable edema and HTN
  • rapid loss of renal function accompanied by oliguria
A

RPcGN

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22
Q

What is the treatment for type 2 RPcGN?

A

steroids and cytotoxic drugs (anti-inflam)

- plasmapheresis only treats type 1

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23
Q

child (or young adult) with massive selective proteinuria, though they have preserved renal function without hematuria or HTN

  • normal glomerulus, but EM shows uniform/diffuse effacement in the visceral epithelial cells of foot processes
  • effectively treated by corticosteroids**
A

Minimal Change Disease (MCD)

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24
Q

What is the most common cause of nephrotic syndrome in children and can be challenged by steroid therapy?

A

MCD

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25
Q

What populations have an increased risk of MCD?

A
  • patients with Hodgkin lymphoma, with T-cell mediated immune defects
  • patients with certain HLA haplotypes associated with atopy
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26
Q

normal glomerulus, EM shows diffuse effacement of foot processes (extra epithelial damage and sclerosis under light microscopy)

  • higher incidence of hematuria and HTN
  • reduced GFR
  • nonselective proteinuria
  • poor response to corticosteroids
A

Focal Segmental Glomerulosclerosis (FSGS)

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27
Q

Podocin (NPHS2) mutation, chromosome 19q13

A

Finnish type FSGS

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28
Q

NPHS2 mutation, chromosome 1q25-q31 (AR)

- steroid resistant pediatric form

A

Podocin FSGS

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29
Q

AD, insidious in onset with high rate of progression to renal insufficiency

A

Alpha-actinin 4 FSGS

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30
Q

Mutation associated with adult onset FSGS?

A

TRP6

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31
Q

chromosome 22, increases the risk of FSGS in African Americans
- also associated with increased resistance to trypanosome infection

A

Apolipoprotein L1

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32
Q

Adults and kids, usually African American

  • retraction/collapse of the entire glomerular tuft, with or without additional lesions
  • proliferation and hypertrophy of glomerular visceral epithelial cells
  • significantly decreased GFR with azotemia, focal IgM and C3 in mesangial distribution, HTN
  • does not respond to corticosteroids**
A

Collapsing glomerulosclerosis

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33
Q

What is the most characteristic lesion of HIV-associted nephropathy?

A

Collapsing glomerulosclerosis

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34
Q

35 year old male presents with nephrotic syndrome and microscopic hematuria, CD4 count >500.

What is he most at risk for infection from?

A

acute pyogenic infection (staph and strep pneumoniae), due to loss of Ig in the urine

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35
Q

adolescents and young adults

  • nephrotic syndrome with a nephritic component, manifested by hematuria and mild proteinuria
  • thickened GBM, showing “tram-track” appearance (splitting) d/t new basement membrane synthesis in response to subendothelial deposits of immune complexes
A

Membranoproliferative Glomerulonephritis (MPGN)

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36
Q

adult patient, mixed nephrotic/nephritic, deposition of iGG and complement
- associated with chronic antigenemia causing immune complex deposition (HepC, SLE, endocarditis, lymphomas)

A

Type 1 MPGN

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37
Q

sicker, nephritic patient

  • alternative complement activation causes a dense deposit
  • C3 found in the GBM, elaborates C3 Nephritic Factor (C3NeF)
  • messangial proliferation with involvement of the basement membrane
A

Type 2 MPGN

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38
Q

immune complex deposition and activation of complement, mostly in adults

  • associated with chronic immune complex disorders: SLE, HepB, HepC, endocarditis, HIV
  • a1-AT deficiency
  • malignant diseases like lymphoid tumors
A

Secondary MPGN (almost always Type 1)

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39
Q

excessive activation of alternative complement pathway and deposition in the glomerulus
- C3 nephritic factor (C3NeF) auto-Ab’s bind C3 convertase, protecting it from INactivation -> promotes persistent C3 activation and subsequent HYPOcomplementemia

A

Dense deposit disease (MPGN Type 2)

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40
Q

What else can dense deposit disease be associated with other than C3NeF?

A

mutations in Factor H

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41
Q
  • kids and yound adults, poor prognosis
  • 50% progression to ESRD
  • reoccurrence in 90% of transplant recipients
  • permeation of the lamina densa of the GBM by an extremely electron dense ribbon of material*
A

Dense deposit disease (MPGN Type 2)

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42
Q

What is the most common cause of glomerulonephritis worldwide?

A

Berger Disease (IgA nephropathy)

  • IgA deposits found in the mesangium, detected by IF with recurring hematuria
  • C3 commonly found in deposits, C1q and C4 are absent
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43
Q

affects any age, especially older kids and young adults

  • pt presents with gross hematuria following an infection of the respiratory of GI tracts
  • bleeding lasts a few days, then comes back every few months
  • microscopic hematuria (30-40%)
  • 5-10% develop acute nephritic syndrome
  • prolonged progression to eventual renal failure (increased risk of progression with old age, heavy proteinuria, HTN and more glomerulosclerosis)
A

Berger Disease

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44
Q

pt presents with gross microscopic hematuria, red cell casts, slowly progressing proteinuria,

  • auditory disturbances
  • vision problems
  • renal failure
  • defective GBM (defect in alpha-5 chain of type 4 collagen synthesis)
A

Alport Syndrome
- X-linked inheritance 85%

NOTE: disease is onset at birth, but symptoms do not occur until later in life

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45
Q

What chromosomes are type 4 collagen genes found on?

A

2, 13, X

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46
Q

What is type 4 collagen crucial for?

A

function of GBM, lens of the eye, and the cochlea

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47
Q

common, asymptomatic hematuria, discovered by routine UA

  • mild/moderate proteinuria, normal renal function, excellent prognosis
  • defect in alpha-3/4 chain of type 4 collagen
  • a5 chain of type 4 collagen IS present -> no ocular or auditory lesions
  • no IgA immune deposition in mesangium
A

Thin Basement Membrane Disease

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48
Q

pt presents with loss of appetite, anemia, vomiting and weakness
morphology shows symmetrically contracted kidneys, diffuse granular cortical surfaces
- thinned cortex, with increase in peri-pelvic fat

A

Chronic Glomerulonephritis

- the end point of all nephrotic and nephritic syndromes

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49
Q

Ab-Ag deposits in glomerular filtration barrier

  • macrophage activation leads to injury and eventual fibrosis of the glomerulus
  • wire-loop appearance
A

Lupus

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50
Q

What is the most common and severe form of Lupus?

A

Class 4

  • > 50% of all glomeruli involved “diffuse”
  • proliferation of endothelial, mesangial and epithelial cells -> lateral crescents that fill Bowman’s space
51
Q

child presents with pruritic skin lesions on extensor surfaces of arms/legs and buttocks, abdominal pain, intestinal bleeding, arthralgia and renal abnormalities
- atopy and URI

A

Henoch-Schonlein Purpura

- excellent prognosis in children, unless omnious clinical signs are present

52
Q

What is Henoch-Schonlein Purpura most likely related to?

What are the main differences?

A

is probably a spectrum of disease related to IgA nephropathy (Bergers)
- Henoch-Schonlein Purpura is systemic, while Berger’s is localized to the kidney

53
Q

pt presents with nephrotic syndrome, hematuria (nephritic) and progressive renal insufficiency

  • EM shows fibrillar deposits in the mesangium and glomerular capillary, that look like amyloid fibrils, but do not stain with Congo red
  • selective deposition of polyclonal IgG (mostly IgG4) and C3 on IF
A

Fibrillary Glomerulonephritis

54
Q

IgG-IgM complexes (cyroglobulins) induce cutaneous vasculitis, synovitis and proliferative glomerulonephritis
- associated with HepC

A

Essential Mixed Cryoglobulinemia

55
Q

Where does Toxin ATI show focal, nonspecific necrosis?

A

straight portion of the proximal tubule and thick ascending limb

56
Q

Eosinophilic hyaline and pigmented granular casts are common, especially in distal tubules and collecting ducts
- casts contain mostly Tamm-Horsfall protein (urinary glycoprotein normally secreted by the cells of the ascending thick limb and distal tubules)

A

Acute Tubular Injury/Necrosis (ATI)

57
Q

What are 7 causes listed of ATI?

A
  1. rhabdomyolysis (myoglobin is released -> nephrotoxic)
  2. aminoglycosides (reserved for life-threatening gram- orgs)
  3. mercuric chloride (large acidophillic inclusions)
  4. carbon tetrachloride (lipid accumulation)
  5. cisplatin and cyclosporine (chemotheraputic agents)
  6. contrast dye (is hyperosmolar -> nephrotoxicity)
  7. crystal deposition -> ballooning of PCT
58
Q

What are the 3 phases of ATI?

A
  1. initiation (36 hours, nephrotoxic insult has not yet caused acute renal failure)
  2. maintenance (sustained decreases in urine output)
  3. recovery
59
Q

What is the diagnostic marker for ATI?

A

dirty brown granular casts aka renal failure casts

60
Q

What is the difference between acute and chronic tubulointerstitial nephritis?

A
  • acute: rapid clinical onset, interstitial edema, WBC infiltration of interstitium and tubules with tubular injury
  • chronic: infiltration with mostly mononuclear WBC’s, fibrosis, lots of tubular atrophy
61
Q

What is the difference between tubulointerstitial nephritis and glomerular disease?

A
  • absence of nephritic and nephrotic syndrome

- presence of defects in tubular function

62
Q

What are the common Gram neg bacteria that cause acute pyelonephritis?

A

E. coli, Proteus, Klebsiella, Enterobacter

- Strep faecalis and staph saprophyticus called “honeyoon bugs” d/t likelihood to cause UTI in sexually active females

63
Q

What organism can cause a caseating granulomatous inflammation?

A

mycobacterium

NOTE: funal infections are non-caseating

64
Q

What is the Vesicoureteral Reflux (VUR)?

A
  • congenital: malformed or incompetent valve
  • acquired: atony of the bladder

They allow bacteria to gain access to the ureters

65
Q

What is the intrarenal reflux?

A

infected bladder urine can be propelled up to the renal pelvis and deep into the renal parenchyma thru open ducts at the tips of the papillae
- most common at upper and lower poles of the kidney

66
Q

morphological hallmarks are: patchy interstitial suppurative inflammation (focal abscesses or large wedge-like areas), intralobular WBC aggregates (WBD casts on UA) and tubular necrosis

A

acute pyelonephritis morphology

NOTE: affects the upper and lower poles most

67
Q

What are the 3 complications of acute pyelonephritis?

A
  1. papillary necrosis
  2. pyonephrosis
  3. perinephric abscess
68
Q

seen in diabetics, sickle cell disease and those with urinary tract obstruction

  • typically bilateral
  • grey-white to yellow necrosis
  • preservation of outlines of tubules with WBCs limited to the preserved and destroyed tissue
A

papillary necrosis

69
Q

seen when there is a total or almost complete obstruction, particularly when it is high in the urinary tract
- severe infection that totally occludes the lumen and outflow with pus that fills the renal pelvis, calyces and ureter

A

pyonephrosis

70
Q

suppurative inflammation that extends through the renal capsule into the perinephric tissue

A

perinephric abscess

71
Q

50 year old male presents with dysuria/frequency with sudden onset of flank pain at the costovertebral angle (flank pain)
- culture shows pathogens, urine shows WBC’s

A

Acute pyelonephritis

  • associated with UTI, VUR, urinary tract instrumentation (catheters), pregnancy and DM
  • more common in males <1 and >40
72
Q

post-transplant (immunocompromised) pt with infection of tubular epithelial cell nuclei

  • nuclear enlargement and intranuclear inclusions (viral cytopathic effect)
  • inclusions arrayed in crystalline-like lattices
A

Pylomavirus nephropathy

73
Q

What is the most common pyelonephritic scarring?

- occurs early in childhood from superimposition of UTI on congenital VUR and intrarenal reflux

A

Reflux nephropathy

74
Q

obstructions predispose pt to infections

  • recurring inflammaition can lead to scarring and chronic pyelonephritis
  • defective posterior urethral valves bilateral
  • coarse, discrete corticomedullary scars overly dilated, blunted or deformed calyces -> flatten the papillae = THYROIDIZATION
A

Chronic obstructive pyelonephritis
- pt presents with back/flank pain, fever, pyuria, bacteremia

NOTE: pts receive medical attention late in disease course because onset is so slow

75
Q

older pt presents with fever, rash, eosinophilia, and acute renal failure (increased serum creatinine and oliguria) approx 15 days after exposure to offending agent
- papillary necrosis with gross hematuria

A

Acute (Drug-Induced) Tubulointerstitial Nephritis

76
Q

How do you treat Acute (drug-induced) tubulointerstitial nephritis?

A

removal of drugs leads to recovery and healing!

- NSAID’s, synthetic penicillins, other synthetic antibiotics

77
Q

What are patients with analgesic nephropathy more likely to develop?

A

urothelial carcinoma of the renal pelvis

78
Q

What is the earliest functional defect seen in hypercalcemia and nephrocalcinosis?

A

inability to concentrate urine

79
Q

What does excess phosphate load lead to?

A

marked precipitation of calcium phosphate > presents as renal insufficiency several weeks later

80
Q

Ig light chains form complexes with Tamm-Horsefall proteins under acidic conditions causing tubular obstruction and inflammation

A

Bence-Jones proteinuria and cast nephropathy

81
Q

What is myeloma kidney?

A

light chain cast nephropathy

- most of the kidney damage is restricted to the tubulointerstitial part

82
Q

older African American pt with diabetes and HTN

- inconspicious proteinuria, decreased GFR, increased risk towards chronic renal failure

A

Nephrosclerosis

83
Q

When would you see hyperplastic changes in renal arteries?

A

Malignant Hypertension Nephrosclerosis

extreme BP -> endothelial cell damage -> increased permeability to fibrinogen -> fibrinoid necrosis -> intravascular thrombosis

84
Q

African American male, DM, HTN, retinal hemorrhages, encephalopathy, CV abnormalities, renal failure

  • early sx: d/t increased intracranial pressure (HA, NV, vision problems)
  • proteinuria, maybe hematuria
  • “flea-bitten” appearance of kidney
A

Malignant HTN Nephrosclerosis

85
Q

What are the two demographics most likely to have Unilateral Renal Artery Stenosis?

A
  1. old diabetic men -> cause by increase Renin production from ischemic kidney
  2. women in their 20-30’s -> fibromuscular dysplasia sting of beads
86
Q

Pt looks like they have essential HTN, bruit can be head on affected kidney, elevated plasma renin, which shows response to ACE-I

A

Unilateral Renal Artery Stenosis

87
Q

What is the definitive therapy for Unilateral Renal Artery Stenosis?

A

Arteriography (to find lesion, then surgery! (after pt has responded well to ACE-I or ARB)

88
Q

What is they cause of Typical Hemolytic-uremia syndrome (HUS)?

A

Shiga-like toxin (E.coli hamburgers, raw milk, and person-person)

89
Q

children and elderly pts, hematememesis and melena, following a flu-like prodrome
- oliguria/hematuria/ hemolytic anemia may follow

A

Typis HUS

- acute setting resolves itself, long term is managed by dialysis, prognosis is poor

90
Q

normal levels of ADAMTS13, inappropriate activation of complement

  • neuro signs/symptoms
  • endothelial injury
  • defects in Factor H, 1 and CD46
A

Atypical HUS

- can develop at any age

91
Q

<40 year old pt presents with fever, neurological symptoms, microangiopathic hemolytic anemia, thrombocytopenia, and renal failure
- deficient in ADAMTS13 (normally regulates vWF)

A

Thrombotic Thrombocytopenic Purpura (TTP)

92
Q

How is TTP treated?

A

plasmapheresis (provides functional ADAMTS13)

93
Q

Subscapular petechiae, thickened capillary walls, mesangiolysis, fibrinoid necrosis and occlusive thrombi

A

HUS/TTP

94
Q

Why should you avoid ACE-I and ARB’s in Atherosclerotic Ischemic Renal Disease?

A

decrease in Ang II will dilate the efferent arteriole -> increasing RBF, but decreasing GFR = acute renal failure

95
Q

What can prevent further decline in renal function in a pt with Atherosclerotic Ischemic Renal Disease?

A

surgical revascularization

96
Q

African American male, with sickle cell and HTN

  • flank pain
  • excreting blood clots
  • insidious onset of hematuria, followed by proteinuria, polyuria, HTN
  • multiple expanding cysts of both kidneys
A

Autosomal Dominant Polycystic Kidney Disease (ADPKD)

97
Q

Where is PDK1 expressed?

A

tubular epithelial cells, particularly those of distal nephron*
- involved in cell-cell and cell-matrix interactions

98
Q

Where is PKD2 expressed?

A

integral membrane protein expressed in all segments of the renal tubules and many extrarenal tissues
- is a Calcium permeable cation channel

99
Q

Where do Intracranial Berry Aneurysms arise from?

A

altered expression of polycystin in vascular smooth muscle

- isolated, basilar subarachnoid hemorrhage in a young patient -> ADPKD

100
Q

highly fatal in infancy, obvious renal failure in all classes, childhood form shows smaller cysts at right angles

  • mutations in PKHD1 on chromosome 6 disrupt the collecting tubule
  • tiny elongated cysts along the interior have a sponge-like appearance when cut
A

Autosomal Recessive Polycystic Disease

101
Q

child pt presents with unexplained renal failure with familial history, large cysts at cortico-medullary junction (small cysts in cortex)

  • polyuria, polydypsia, Na wasting and tubular acidosis
  • renal failure in 5-10 years
A

Medullary Sponge Kidney

102
Q

What is associated with renal cell carcinoma from the walls of cysts?

A

Acquired (dialysis associated) cystic disease

- pts on hemodialysis for a long period of time have an increased incidence of RCC

103
Q

When are calcium phosphate stones more common than calcium oxalate stones?

A

in the general population

104
Q

What are calcium oxalate stones more common than calcium phosphate stones?

A

in pt’s receiving renal dialysis

105
Q

Which stone type is associated with hypercalciuria, with or without hypercalcemia?

A

Calcium Oxalate Stones

- is a result of hyperparathyroidism, renal impairment of calcium reabsorption or hyper-absorptive intestinal tract

106
Q

What is seen in diarrhea and metabolic acidosis?

A

hypocitraturia

- may also lead to calcium stones

107
Q

What type of stone is made from Magnesium ammonium phosphate

  • caused by urea-splitting bacteria
  • is the largest kidney stone
A

Struvite Stones

- Staghorn Calculi

108
Q

What type of stone mostly occurs unilaterally at the renal calyx, pelvis or the bladder

  • vary in size (<5mm small, .7mm large)
  • form staghorn calculi
  • present in younger pt’s (20/30’s), show familial patterns
  • cause renal colic, sharp flank pain that radiates to groin, and hematuria
A

Cystine Stones

109
Q

Small (<5cm), pale, yellow-gray, well-circumscribed nodules within the cortex

  • complex branching papillomatous structure with complex fronds
  • cuboidal to polygonal in shape, with regular, small, central nuclei, little cytoplasm, and no atypia
A

Renal Papillary Adenoma (benign)

NOTE: potentially malignant at any size, but especially if greater than 3cm (consider all adenomas as potentially malignant)

110
Q

benign neoplasm consisting of vessels, smooth muscle, and fat from the perivascular epithelioid cells

  • likely to spontaneously hemorrhage
  • associated with Tuberous Sclerosis**
  • loss of function mutations in TSC1/2
  • lesions of cerebral cortex that produce epilepsy, retardation, skin problems
A

Angiomyolipoma (aka Renal Fibroma, or Hamartoma)

111
Q

epithelial neoplasm composed of large, eosinophillic cells with small, round benign-looking nuclei that have large nucleoli

  • comes from intercalated disks of collecting ducts
  • massive amounts of mitochondria
  • tan/brown tumors well-circumscribed with a central scare
A

Oncocytoma

112
Q

What is the greatest risk factor for Renal Cell Carcinoma?

A

smoking

  • also HTN, obesity, unopposed estrogen therapy
  • exposure to asbestos, heavy metals
113
Q

AD inheritance

  • mutations in FH gene (fumarate hydratase)
  • cutaneous and uterine leiomyomata with an aggressive type of papillary carcinoma
A

Hereditary Leiomyomatosis/Renal Cell Cancer Syndrome

114
Q

AD inheritance

  • mutations in MET proto-oncogene
  • many bilateral tumors with papillary histology
A

Hereditary papillary carcinoma

115
Q

What is the most common type of renal cell carcinoma?

A

Clear cell carcinoma

  • 98% caused by loss on chromosome 3 where VHL gene is
  • inappropriate expression of genes turned on by HIF-1 promotes angiogenesis (VEGF) and stimulate grown IGF-1)
116
Q

Nonpapillary, unilateral tumors

  • large clear or granular cells
  • bright yellow-white-grey tumors
  • tumors are typically differentiated
  • likely to invade renal vein -> IVC -> heart
  • can cause a varicocele if located on LEFT
A

Clear Cell Carcinoma

117
Q

multifocal origin tumor,

  • sporadic: trisomies 7 and 17, loss of Y in males
  • familiar: just trysomy 7
  • cancer associated with dialysis-associated cystic disease
  • not associated with chromosome 3p deletions (like VHL and clear cell are)
  • cuboidal or columnar epitheliumm arranged in papillary pattern
A

Papillary Carcinoma

118
Q

young pt

  • translocations of TFE3 gene
  • cells have clear cytoplasm with papillary architecture
A

Xp11 translocation carcinoma

119
Q

often asymptomatic, discovered by CT/MRI for nonrenal cause

  • may reach massive sizes before symptoms set in
  • triad of symptoms: hematuria**, flank pain, and mass
A

Collecting duct (Bellini duct) carcinoma

120
Q

What is the recommended treatment for a T1a tumor (<4cm) causing paraneoplastic syndromes?

A

partial nephrectomy

121
Q

What are the 3 stages of paraneoplastic syndome?

A

Stage 1: only 1 kidney involved
Stage 2: kidney and far are involved
Stage 3: kidney and renal vein or lymph are involved

122
Q

What is the main risk factor for urothelial carcinoma of the pelvis?

What other disorders are they associated with?

A
  • smoking

- Lynch syndrome and analgesic nephropathy

123
Q

What tumors are typically found early, as they produce painless hematuria?

A

Urothelial carcinoma of the pelvis

NOTE: may block urine outflow and lead to hydronephrosis and flank pain

CPR II Exam 2 (5 decks)

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