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Pathology Pt. 4 > Kidneys, Urinary > Flashcards

Kidneys, Urinary Flashcards

1
Q

Name three developmental disorders of the kidneys.

A
  1. Renal agenesis
  2. Horseshoe kidney
  3. Ectopic kidney
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2
Q

What is renal agenesis? What are the symptoms?

A

It is complete absence of renal tissue. Can be unilateral or bilateral. Unilateral is usually asymptomatic and the remaining kidney udergoes compensatory hypertrophy. Bilateral is fatal (Potter syndrome).

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3
Q

What is Potter syndrome?

A

Bilateral renal agenesis - fatal

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4
Q

What is horseshoe kidney? What are some complications?

A

When the kidneys fail to separate at the lower poles during development. The kidneys are unable to ascend past the inferior mesenteric artery due to the abnormal connection so they are found inferior to this artery. Can potentially compress the vena cava, aorta, or urinary tract.

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5
Q

What is ectopic kidney? What are some complications?

A

A birth defect in which a kidney is located below, above, or on the opposite side of its usual position. They are prone to infection or obstruction.

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6
Q

What is the etiology of hereditary cystic diseases of the kidneys?

A

A defect in the cilia-centrosome complex of renal tubular epithelial cells. This leads to altered growth of the epithelial cells and abnormal fluid and ECM secretion.

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7
Q

Describe a “simple cyst” of the kidney.

A

Benign, 1-5 cm, translucent, with clear fluid.

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8
Q

What is the etiology of Autosomal Dominant (Adult) Polycystic Kidney Disease (ADPKD)?

A

A defect in the cilia-centrosome complex of renal tubular epithelial cells.

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9
Q

What are the two main roles of the ciliated epithelial cells of renal tubules?

A
  1. Sense urine flow

2. Regulate tubule growth

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10
Q

What are the two gene mutations involved in autosomal dominant polycystic kidney disease? What are the protein products of these genes?

A

85% have mutations in PKD1 and 15% have mutations in PKD2. Products are polycystin-1 and polycystin-2 which are needed for proper ciliary function.

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11
Q

Describe the morphological changes seen in autosomal dominant polycystic kidney disease (5).

A
  1. Both kidneys are extremely enlarged.
  2. Irregular surface.
  3. Tons of cysts 3-4 cm in diameter filled with fluid.
  4. Little parenchyma between cysts due to ischemic atrophy from pressure of surrounding cysts.
  5. Asymptomatic cysts in the LIVER found in 1/3 of patients.
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12
Q

Describe the clinical features of autosomal dominant polycystic kidney disease (8).

A
  1. Asymptomatic until 4th decade - onset of renal failure.
  2. Flank pain (above your hips).
  3. Bilateral flank and abdominal masses.
  4. Sense of heaviness in the loins.
  5. Intermittent gross hematuria.
  6. Hypertension in 75% of patients.
  7. UTI
  8. Azotemia (elevated BUN)
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13
Q

Which is more common: autosomal recessive polycystic kidney disease or autosomal dominant polycistic kidney disease?

A

Autosomal dominant (1 in 400-1,000 births)

Autosomal recessive is 1 in 20,000 births

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14
Q

What gene mutation causes autosomal recessive polycystic kidney disease and what is its gene product?

A

Caused by a mutation in the PKHD1 gene. The gene product is fibrocystin which is needed for proper ciliary function of the tubular epithelial cells.

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15
Q

What is the prognosis for autosomal recessive polycystic kidney disease?

A

75% of infants die in the perinatal period, often from pulmonary hypoplasia (failure of lung development) due to low amniotic fluid, hepatic failure, or renal failure. Those that survive go on to develop liver cirrhosis.

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16
Q

Name the condition with the following characteristics:

  1. Numerous small cysts in the cortex and medulla of the kidneys.
  2. External surface of the kidneys are SMOOTH.
  3. Cysts are fusiform dilations of cortical and medullary collecting ducts with a radial arrangement.
  4. Cysts lined by cuboidal epithelial cells.
  5. Interstitial fibrosis and tubular atrophy seen.
  6. Liver is fibrotic.
A

Autosomal recessive (childhood) polycystic kidney disease.

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17
Q

What causes glomerulonephritis?

A

Deposition of immune complexes in the glomeruli.

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18
Q

Glomerulonephritis may cause proliferation of ________, ________, and ________ cells in the kidneys.

A

endothelial, mesangial, and epithelial cells

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19
Q

What is the clinical syndrome called that glomerulonephritis causes? What are the clinical manifestations of this syndrome (10)?

A

Nephritic syndrome, characterized by:

  1. Hematuria (acute, grossly visible).
  2. Proteinuria
  3. Decreased GFR
  4. Elevated BUN
  5. Elevated serum creatinine
  6. Oliguria (low urine output)
  7. Salt and H2O retention
  8. Hypoalbuminemia
  9. Edema
  10. Hypertension
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20
Q

How can group A streptococcal infection cause glomerulonephritis, leading to nephritic syndrome?

A

Circulating strep antibodies get trapped in glomeruli, bind complement, recruit leukocytes and inflammatory cells –> necrosis of glomeruli

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21
Q

Which specific antibodies and complement proteins are found in the glomeruli in the case of acute poststreptococcal gomerulonephritis in the early stage vs in the late stage?

A

Early: coarse, granular deposits of IgG and C3
Late: C3 deposits

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22
Q

What cellular changes are seen in the case of acute poststreptococcal gomerulonephritis (5)?

A
  1. Diffuse glomerular enlargement and hypercellularity (caused by intracapillary leukocytes).
  2. Proliferation of endothelial, mesangial and parietal cells.
  3. Infiltration of neutrophils and monocytes.
  4. Subepithelial immune complex deposits (isolated HUMPS between the outer surface of the glomerular basement membrane and the podocytes).
  5. Subendothelial deposits in the mesangium, between the endothelial cells and the glomerular basement membrane.
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23
Q

In acute poststreptococcal glomerulonephritis, ____% of children recover without complications and it is one of the ______ common childhood renal diseases.

A

90% recover, one of the most common childhood renal diseases

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24
Q

Acute poststreptococcal glomerulonephritis can cause ____-lived nephritic syndrome, which is characterized by ______, ______, ______, and ________. Additionally, _______ and facial edema may persist for several months.

A

short-lived nephritic syndrome, characterized by oliguria (low urine output), azotemia (high levels of nitrogen-containing compounds in blood), hematuria, and hypertension.

Proteinuria and facial edema may persist for several months.

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25
Q

How long does it take for the complement deposits to be cleared from the glomeruli after a case of acute poststreptococcal glomerulonephritis?

A

2 months

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26
Q

What is rapid progressive (crescentic) glomerulonephritis characterized by both clinically and cellularly?

A

Characterized clinically by having features of nephritic syndrome and rapid loss of renal function.

Cellular changes include glomerular necrosis, inflammation, wrinkling and breaks in the glomerular basement membrane, and proliferation of parietal epithelium (crescents) of Bowman’s capsule.

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27
Q

What causes anti-glomerular basement membrane (Type 1) crescentic glomerulonephritis?

A

Auto-reactive antibodies against the alpha-3 type of collagen IV in the glomerular basement membrane

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28
Q

What is Goodpasture syndrome?

A

A condition that causes anti-glomerular basement membrane (Type 1) crescentic glomerulonephritis and also includes antibody attack of the basement membrane in the lungs.

Note that anti-BM T cells may also play a role

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29
Q

Which HLA type is associated with anti-glomerular basement membrane disease?

A

HLA-DR2

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30
Q

Name the disease:

  1. Enlarged and pale kidneys with petechial hemorrhages on the cortical surfaces.
  2. Segmental necrosis and breaks in the GBM.
  3. Proliferation of parietal epithelial cells and migration of monocytes and macrophages that form crescents filling Bowman’s space.
  4. Strong, diffuse LINEAR staining of the glomerular basement membrane for IgG and C3 with immunofluorescence.
  5. Fibrin strands between cellular layers in the crescent.
  6. Eventual scarring and glomerulosclerosis.
A

Anti-glomerular basement membrane (Type 1) crescentic glomerulonephritis.

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31
Q

Anti-Glomerular Basement Membrane (Type I) Crescentic Glomerulonephritis accounts for ____ to ____% of rapid progressive (crescentic) glomerulonephritis.

A

10-20%

32
Q

What is the treatment for Anti-Glomerular Basement Membrane (Type I) Crescentic Glomerulonephritis? What happens if it is untreated?

A

Tx includes immunosuppressive therapy and plasmapheresis (removes Igs from circulation), or kidney transplantation.

If untreated, the patient dies in weeks to months from renal failure.

33
Q

What causes acute tubular necrosis? Is it reversible?

A

Caused by ischemia (hypovolemia, MI, or endotoxic shock) or toxic injury (ethylene glycol, mercuric chloride, gentamicin, CCL4, etc.). It is reversible.

34
Q

What is the mechanism by which GFR decreases in the case of acute tubular necrosis?

A

Necrosis and sloughing of tubular epithelial cells causes an obstruction in the tubules. Tubuloglomerular feedback senses this and causes afferent arterioles to constrict so that blood is shunted away from the damaged tubule –> decreased GFR.

35
Q

What morphological changes are seen in the case of acute tubular necrosis (8)?

A
  1. Prominent injury in the straight part of the proximal tubules and thick loop of Henle.
  2. Flattened epithelium.
  3. Dilation of the lumen.
  4. Loss of brush border.
  5. Proteinaceous CASTS made of TAMM-HORSFALL protein normally secreted by tubular epithelium + other proteins found in the distal tubules and collecting ducts.
  6. Short, segmental necrosis.
  7. Sloughing of individual epithelial cells and denuding of the BM leads to backleaks.
  8. Congested vasa recta of the outer medulla with monocyte infiltrate.
36
Q

What are the clinical features of acute tubular necrosis (3)?

A
  1. Rapidly rising serum creatinine.
  2. Oliguria
  3. Urinalysis shows degenerating epithelial cells and dirty brown granular casts made of tubular proteins and Hb.
37
Q

How is a urinary tract infection diagnosed/confirmed clinically?

A

When urinalysis shows bacterial colonies in excess of 100K/ml and the presence of white blood cells (mostly polymorphs).

38
Q

What are the two ways in which infections can spread to the urinary tract? Which is more common?

A

Ascending (from the outer periurethral area) or hematogenous.

Ascending is more common.

39
Q

Name 11 conditions that are predisposing to ascending UTI.

A
  1. Urinary stones
  2. Congenital megaureter
  3. Strictures
  4. Pregnancy
  5. Tumors (mass effect)
  6. Vesicoureteral sphincter incompetence –> reflux
  7. Incompetence
  8. Chronic cystitis
  9. BPH
  10. Females (short urethra)
  11. Insertion of a catheter/instrumentation
40
Q

Ascending UTI will cause a combination of urinary bladder infection, _________ reflux, and _________ reflux.

A

urinary bladder infection, vesicourethral reflux, and intrarenal reflux

41
Q

What is acute pyelonephritis?

A

A complication of bacterial UTI that is characterized by supperative inflammation of the kidney and the renal pelvis.

42
Q

Name six bacteria that can cause acute pyelonephritis.

A
  1. E. coli
  2. Klebsiella
  3. Enterobacter
  4. Proteus
  5. Pseudomonas
  6. Serratia
43
Q

What factors predispose someone to acute pyelonephritis?

A

The 11 things that predispose people to UTIs + things like genetics, outflow obstruction, vesicoureteral reflux or intrarenal reflux.

44
Q

Describe five morphological changes seen in acute pyelonephritis.

A
  1. Extensive FOCAL inflammatory destruction in the parenchyma of the cortex (but somehow sparing vessels and glomeruli).
  2. Abscesses on the subcapsular surface and on cut surfaces.
  3. Neutrophils infiltrating the tubules and collecting ducts.
  4. Necrosis of papillary tips and perinephritic abscesses.
  5. Obstruction –> pus in the renal pelvis and calyces –> pyonephrosis.

Easier: abcesses, neutrophils, pus, focal destruction of cortex but not glomeruli

45
Q

What are the clinical features of acute pyelonephritis (6)?

A
  1. Typical signs of bacterial infection (fever, chills, sweats, malaise, etc.).
  2. Dysuria
  3. Bacteruria
  4. Flank pain
  5. Leukocytosis and neutrophilia
  6. Presence of leukocyte casts in the urine

Easier: Leukocytes in piss and blood, neutrophils in blood. Pissing hurts, sides hurt, feel like shit overall.

46
Q

A Wilms Tumor is a malignant neoplasm of the ________ composed of ________ elements with a mixture of _______, ______, and _______ tissue.

A

malignant neoplasm of the kidneys composed of embryonal elements with a mix of blastemal, stromal, and epithelial tissue

47
Q

What tumor type is the most frequent abdominal solid tumor in children (prevalence of 1 in 10,000)?

A

Wilms Tumor of the kidney

48
Q

____% of Wilms tumor cases are sporadic and unilateral, while ____% are associated with defects of the _____ gene located on chromosome 11 (11p13).

A

90% are sporadic and unilateral

10% are associated with WT1 gene defects

49
Q

What does the WT1 gene do?

A

It is a tumor suppressor that regulates the transcription of other genes

50
Q

Describe three morphological characteristics and three clinical features of a Wilms tumor.

A

Morphological:

  1. Tumor is large by the time of detection.
  2. Kidney has a bulging, pale-tan cut surface enclosed with a thin rim of renal cortex and capsule.
  3. Tumor contains elements that resemble normal fetal tissue including metanephric blastema, immature stroma, and immature epithelial elements.

Easier: large, tan, all sorts of fetal type stuff

Clinical:

  1. Usually presents between 1-3 years old.
  2. 98% occur before age 10
  3. Palpable abdominal mass, pain, intestinal obstruction, hypertension, hematuria.
51
Q

How is a Wilms tumor treated?

A

Combination of surgery, chemo, radiation.

52
Q

What is the most common primary cancer of the kidney? Describe it.

A

Renal cell carcinoma: a malignant neoplasm of renal tubular or ductal epithelial cells.

53
Q

Renal cell carcinomas account for ___% of all renal cancers and more than 30,000 cases per year in the U.S.

A

80%

54
Q

At what age are and gender are renal cell carcinomas most commonly seen?

A

Men between 50-70 years old

55
Q

Most cases of renal cell carcinoma are ______, with associated loss of the ______ tumor supressor gene.

A

sporadic with loss of the VHL (von Hippel-Lindau) tumor suppressor gene.

56
Q

What are the hereditary forms of RCC?

A

Autosomal dominant and von Hippel-Lindau disease, chromosomal translocation involving 3p, VHL mutations.

57
Q

Which type of renal cell carcinoma is not associated with the VHL gene?

A

Hereditary papillary carcinomas.

58
Q

What is the most common variant of renal cell carcinoma? From what cell does it arise from?

A

Clear cell renal cell carcinoma - arises from proximal tubular epithelial cells.

59
Q

Describe a clear cell RCC tumor (5).

A
  1. Yellow-orange mass with focal hemorrhage and necrosis.
  2. Tumor is solid or focally cystic.
  3. Neoplastic cells have clear cytoplasm.
  4. Tumor cells arranged in round or elongated collections surrounded by a network of delicate vessels.
  5. Little cellular or nuclear pleomorphism.

Easier: yellow, focal, solid or cystic, homogenous, round arrangement.

60
Q

What are the clinical features of renal cell carcinoma (5)? Which signs are included in the “triad of presenting feeatures?”

A
  1. Hematuria - single most common presenting sign.
  2. Flank pain
  3. Palpable mass
  4. Paraneoplastic syndrome common.
  5. Hematogenous spread is early and frequent.

The first three are considered the “triad.”

61
Q

What is the most important prognostic factor in renal cell carcinoma? What is the 5-year survival rate?

A

Tumor stage is most important prognostic factor.

5-year survival rate is 90% if the tumor has not extended beyond the renal capsule.

5-year survival is only 30% if there is distant metastasis.

62
Q

Where exactly do most urinary tract tumors occur? At what age are they most often seen? In which gender?

A

In the urinary bladder. Seen in older patients (median age is 65) and are rare in people under 50. Male:female is 3:1

63
Q

What cell type is most often neoplastic in the case of urinary bladder tumors? What are the rare types?

A

Urothelial cells (transitional epithelium)

Rare types are squamous cell carcinomas, adenocarcinomas, neuroendocrine carcinomas, and sarcomas.

64
Q

True or false: urinary bladder tumors often recur following surgical treatment.

A

True

65
Q

Urinary bladder tumors are often _______ and can occur in any part of the urinary tract that is lined by urothelium.

A

multifocal

66
Q

What is the most important risk factor in the development of a urothelial carcinoma? Name four other factors.

A

Smoking is most important factor.

Others:

  1. Industrial exposure to azo dyes.
  2. Schistosomiasis
  3. Drugs
  4. Radiation therapy
67
Q

Can urothelial carcinomas vary from small, delicate, low-grade papillary lesions limited to the mucosal surface, to larger, higher-grade, solid invasive masses, which are often ulcerated?

A

Yeah

68
Q

How are urothelial carcinomas classified?

A

Either as low or high grade papillary urothelial carcinomas.

69
Q

What are the two symptoms of urothelial carcinomas?

A

Sudden hematuria and dysuria

70
Q

At the time of initial presentation, ____% of urothelial carcinoma cases are confined to the urinary bladder, while ____% have already metastasized.

A

85% are confined, 15% have metastasized

71
Q

Urothelial carcinomas of the renal papilla that are limited to the mucosa or lamina propria are commonly treated by ______ _______.

A

transurethral resection (an endoscopic-type procedure)

72
Q

How are advanced stage urothelial carcinomas treated?

A

Radical cystectomy

73
Q

What are the four morphological types of urothelial carcinomas?

A
  1. Papillary carcinoma
  2. Invasive papillary carcinoma
  3. Flat non-invasive carcinoma (CIS)
  4. Flat invasive carcinoma
74
Q

What are the three main locations where kidney stones get stuck?

A
  1. Uretopelvic junction (exiting the kidneys)
  2. Crossing of the iliac artery (in the middle of the ureter)
  3. Uretero-vesical junction (right before it goes into the bladder)
75
Q

True or false: urothelial carcinomas are staged according to the TNM classification.

A

True

Pathology Pt. 4 (10 decks)

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