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DT3-Exam 3 > Obstructive Disease-- Melissa* > Flashcards

Obstructive Disease-- Melissa* Flashcards

1
Q

Describe how obstruction causes renal pathology; what is the name of the dangerous phenomenon that can ensue?

A

Obstruction of urine flow–> Infection/ calculi –> HYDRONEPHPHROSIS (dilation of renal pelvis/ calyces; atrophy)

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2
Q

Define Hydronephrosis:

A

dilation of renal pelvis/ calyces + atrophy of kidney due to obstruction of urine outflow

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3
Q

What are some causes of obstruction?

A

Anything that stops urine flow (Calculi, tumors, BPH, neurogenic bladder, inflammation…)

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4
Q

How does acute obstruction present? Which size calculi would be most painful if causing obstruction?

A

painful; small stones are most painful (lodge in ureter)

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5
Q

How does bilateral complete obstruction present?

A

oliguria, anuria

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6
Q

How does unilateral complete or partial obstruction present?

A

Hydronephrosis or silent

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7
Q

Which population gets renal calculi most? Are they typically bilateral or unilateral?

A

Young adult males; typically unilateral

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8
Q

What are three potential causes of renal calculi?

A
  • Familial (inborn error of metabolism)
  • Supersaturated urine (^conc. stone stuffs; low volume)
  • Bacterial infection
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9
Q

Calcium Oxalate PO4 Calculi:

Prevalence? #1 cause? Appearance?

A

70% all calculi (Most common!)
#1 cause: Idiopathic Hypercalcinuria
Stones are radiopaque octahedron crystals

(O)xalate =(O)ctahedron

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10
Q

What are some other potential causes of Calcium Oxalate & PO4 Calculi? (4)

A
  • All hypercalcemic states and acidic states
  • Hyperoxaluria (vegetarians)
  • Hyperuricosuria
  • Hypocitraturia
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11
Q 
Struvite calculi: 
Prevalence? 
#1 Cause? 
What do crystals look like? 
What classic finding might struvite stones cause? 
How does step love to ask about this?
A

15-20% all calculi
#1 cause: PROTEUS & Staph (urea splitting bacteria)
*Look for vignette with chronic UTI and ABX use
Crystals: Three to six sided “coffin lids”
After SIX PROTEUS infections, you might be laying in a COFFIN.

IMPORTANT: THESE MAY CAUSE STAGHORN CALCULI!!! ON CT, THESE LOOK LIKE OPACITIES FILLING ALL OF THE RENAL CALYCES. IMPORTANT FOR THIS, MEADOWS, AND STEP!

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12
Q

Describe how struvite calculi form:

A

Proteus: Urea–> ammonia–>ALKALINE URINE–> Mg/AmmoniumPO4 salts precipitate

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13
Q 
Uric Acid calculi:
Prevalence? 
#1 cause? 
Acidic vs basic? 
Stone/ Crystal appearance?
A

5-10% all calculi

  • # 1 Cause: Hyperuricemia (Gout)
  • Remember that most chemo drugs cause gout!!!*
  • Acidic pH
  • Stones are radioLUCENT
  • Crystals are flat, 4 sided, lemon shaped

FOUR LEMONs have a lot of ACID.

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14
Q 
Cystine Calculi: 
Prevalence?
#1 Cause? 
Acidic vs. Basic? 
Describe the crystals.
A

~2% of all calculi

  • # 1 cause = genetic defects in renal absorption of AA
  • Acidic pH
  • Crystals are hexagonal and laminated
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15
Q

Are benign renal tumors more urothelial or renal cell tumors? Are they usually symptomatic? Found in kids or adults?

A

More urothelial; usually incidental findings; usually in adults unless genetic disease (tuberous sclerosis); this may just be because adults have more imaging etc –> asymptomatic tumors are naturally less likely to be detected in kids.

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16
Q

Renal papillary adenoma:
Common cause?
Defining size?

A
  • Associated with long term hemodialysis/Cystic disease

- Clearly benign; less than 0.5cm

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17
Q

What gene mutation is associated with renal papillary adenoma?

A

Lacks 3p alteration

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18
Q

Renal Fibroma/Hamartoma:
Macro path (What is defining size)?
Micro path?

A
  • Macro: Gray-white nodule less than 1 cm in the renal pyramids
  • Micro: collagen and fibroblasts trap tubules/ cement them in!
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19
Q

Angiomyolipoma:
How common are these tumors?
With what disease are these tumors associated?
Describe the macro and micro path.

A
  • Rare
  • Macro: thick walled blood vessels, smooth muscle, fat
  • Micro: spindle and epithelioid cells
  • When multiples think Tuberous Sclerosis (AD)
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20
Q

What are two gene mutations associated with tuberous sclerosis (2)?
What are some other anomalies associated with the disease other than renal angiomyolipomas?

A

AD LOF mutations:
-Chrom 9, TSC1
-Chrom16, TSC2
Lesions in cerebral cortex, skin, heart etc.

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21
Q

Oncocytoma:
Population?
Macro and micro path?

A
  • Old Men
  • Macro: MAHOGANY brown w/ FIBROSIS
  • Micro: small eosinophilic (pink) cells w/ prominent nucleoli
22
Q

List the 4 benign tumors of the kidney:

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

Incidental findings, adults, small.

23
Q

What is a stag horn calculi?

A

large stones fill pelvis +/- calyces

Caused by urea splitting bacteria; i.e. proteus/ staph

24
Q

What is a colic calculi?

A

smaller stones passed into ureter = painful; common in young males

25
Q

Describe the T1-T4 stages of renal malignancy:

A

T1: LESS than 7cm, kidney only
T2: GREATER than 7cm, kidney only
T3: Invades veins, adrenals, perinephric tissue
T4: Invades Grerota’s fascia and beyond

26
Q

Two types of malignant tumors of the kidney:

A 
Renal cell Ca (renal tubular epi)
Urothelial Ca (renal pelvis; urothelium; similar to bladder)
27
Q 
#1 risk for renal cell ca?
#1 population for renal cell ca?
Are they typically sporadic or familial?
A 
#1 risk =TOBACCO
#1 population: male smokers 
Tumors are typically sporadic
28
Q

What is the #1 site for renal cell ca mets?

A 
#1 site = LUNG 
*25% initially present with mets
29
Q

Clinical triad for renal cell ca?

A 
Clinical Triad (10%): 
1.Costovertebral tenderness
2.Palpable mass
3.Hematuria 
(intuitive)
30
Q

How are renal cell ca’s treated?

A

Treatment:

Partial or complete nephrectomy (depends on stage)

31
Q

5 types of renal cell ca + prevalence:

A
  • Clear Cell (80%)
  • Papillary (under 15%)
  • Chromophobe (5%)
  • Collecting Duct
  • Xp11

Clear cell most common; all others rare.

32
Q

Clear Cell:
Population?
Commonly associated genetic disorder?
Micro path?

A

-Adult tumor
-Associated with Von Hippel-Lindau Disease (AD)
Micro: tumor cells with glycogen + lipid–> clear cytoplasm

33
Q

What are some manifestations of VHL disease?? (6)

What is the genetic problem?

A

Von Hippel-Lindau Disease (AD)–>

  • Retina and Cerebellar hemangioblastomas
  • Pancreatic, hepatic
  • renal cysts; Pheochromocytoma

Mutation: Deletion of VHL gene on Chrom 3p

34
Q

Two types of papillary renal cell ca and their genetic mutations:

A

Sporadic

  • Trisomy: 7, 16, or 17
  • Loss of Y in males

Familial
-Trisomy 7; MET GOF mutation (TK receptor)

35
Q

Papillary renal cell ca:
Population?
With what medical procedure are these tumors associated?
Macro and micro path?

A
  • Adult Tumor; commonly associated with dialysis
  • Macro: Multicentric tumor
  • Micro: Many papilla; foamy histiocytes; psammoma bodies (Ca++ deposits)
36
Q

Chromophobe renal cell ca:
Population
Micro path
Common stain used?

A
  • Adult Tumor
  • Micro: Prominent cell membrane; pale eosinophilic cytoplasm; Perinuclar HALO
  • Stains blue on Hale’s Colloidal Iron
37
Q

Collecting duct renal cell ca:
Population/ Prognosis?
Micro path?

A
  • Aggressive Adult tumor; does not respond to chemo; poor prog.
  • Micro: Desmoplastic stroma; tubulopapillary architecture; HOBNAIL CELLS (protruding nuclei)
38
Q

Xp11 renal cell ca:
Population
Micro path

A
  • Younger patients

- Micro: looks similar to clear cell ca. but w/ papillary architecture (fibroblastic core w/ papillary projections)

39
Q

Was is the translocation associated with Xp11 renal cell ca?

A

TFE3 gene translocation–> ^ TFE3 transcription factor

40
Q

From what tissue do urothelial ca of the renal pelvis arise and to what tumor are they similar?
]

A

-Arise from urothelium of renal pelvis (like bladder tumors)

41
Q

Wilms tumor is what kind of kidney tumor?

A

Urothelial tumor; malignant; in kiddos!

Rx question; asked about chromosome 11 mutation.

42
Q

Wilms tumor:
Population
Macro and micro path (3 cell types)

A
  • 2-5yoa (#4 pediatric malignancy)
    Macro: Large round tumor
    Micro: Poorly differentiated BLASTEMA cells; STROMAL cells; EPITHELIAL cells (3 cell types)
43
Q

Anaplasstic Wilms tumors are associated with what genetic anomaly?
What is the prognosis for these tumors?
What is the prognosis for a regular films tumor?

A

Anaplastic tumors= p53 mutations

  • Anaplastic tumors can be resistant to chemo and have bad prognosis
  • Regular wilms tumors have good prognosis with chemo and surgery
44
Q

WAGR SYNDROME:
Genetic mutations (2)
Clinical triad

A

Chrom 11
WT1 gene: Wilms deletion
PAX gene: Aniridia deletion

Clinical Triad (33% develop Wilms Tumor):

  • Aniridia (no iris!)
  • Genital anomalies
  • Mental retardation
45
Q

DENYS DRASH SYNDROME:
Genetic mutations
Clinical triad?

A

WT1 gene: defective DNA binding properties

Clinical triad:

  • 90% have Wilms Tumor
  • Gonadal dysgenesis (male pseudohermaphroditism)
  • Early onset nephropathy w/ diffuse mesangial sclerosis
46
Q

Bechwith –Wiedmann Syndrome (BWS):
Genetic mutations?
Salient clinical features (2)?

A

Chrom 11–> WT2 gene mutation (distal to WT1)

Patients have Wilms tumor and organomeagly

47
Q

Hyper acute Rejection:
Timing
Gross and micro path
Treatment

A

Min/ Hrs
-Gross: Cyanotic, mottled flaccid organ
-Micro: Fibrin thrombi, WBCs
Clinical: MUST REMOVE KIDNEY

48
Q

Acute Cellular Rejection:
Timing
Mediator + micro path
Prognosis

A

Days/Wks
-T CELL MEDIATED (CD4, CD8)
-Micro: Interstitial mononuclear infiltrate; edema; parenchymal injury
Clinical: Responds to prompt ^immunosuppressive therapy

49
Q

Acute Humoral Rejection/ Rejection vasculitis:
Timing
Mediator + micro path
Prognosis

A

Days/Wks
-B CELL MEDIATED (Igs)
-Micro: necrotizing vasculitis; neutro infiltrate; fibrin thrombi; deposition of C4d (classical complement)
Clinical: Treat with B cell depleting agents

50
Q

Chronic Rejection:
Timing
Micro path
Clinical features and prognosis

A

Mos/Yrs
-Creatinine ^ progressively over 4-6 mos
-Micro: glomerular hyalinization; tubular atrophy + chronic inflammation
Clinical: does NOT respond to immunosuppressive therapy u

51
Q 
Tumor assc with VHL 
Tumor assc with Tuberous sclerosis 
Tumor assc with chrom 11 
Tumor assc with TFE3
Tumor assc with MET GOF
A

VHL: Clear Cell
TS: angiomyolipoma
Chrom 11: Wilms
TFE3: Xp11 Renal carcinoma
MET GOF: Familial Papillary Renal Carcinoma
(NOTE: Sporadic is trisomy 7, 16, 17 or Y deletion)

DT3-Exam 3 (9 decks)

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