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Unit 5 > Pathology - renal > Flashcards

Pathology - renal Flashcards

1
Q

Horshoe kidney

A
  • most common congenital anomaly
  • Conjoined kidneys usually located at the lower pole Kidney gets caught on the inferior mesenteric artery (IMA) root during its ascent from pelvis to abdomen
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2
Q

Where (anatomically) are horshoe kidneys found? why?

A

Typically at the lower pole because kidney gets caught on the inferior mesenteric artery (IMA) root during its ascent from pelvis to abdomen

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3
Q

Most common congenital anomaly

A

Horshoe kidney

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4
Q

Where does the kidney develop in normal embryology?

A

Normally develops in the pelvis and ascends to the abdomen

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5
Q

Renal agenesis

A
  • Absent kidney formation – may be unilateral or bilateral
    • Unilateral agenesis --> hypertrophy of the existing kidney –> hyperfiltration increases risk of renal failure later in life
    • Bilateral agenesis –> oligohydramnios which can cause lung hypoplasia, flat face w/ low set ears and development defects of the extremeties (Potter sequence)
      • incompatible with life
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6
Q

Pathogenesis of unilateral renal agenesis

A

Unilateral agenesis –> hypertrophy of the existing kidney

  • Hypertrophy is not a problem until later in life when hyperfiltration can increase the risk of renal failure
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7
Q

Pathogenesis of bilateral renal agenesis

A

Amniotic fluid (AF) is essentially the filtrate coming from the kidney (baby is basically floating in its own urine)

Without kidneys, there will be little AF == oligohydramnios.

Without the cushioning of AF then the baby will be pressed up against the mother’s uterus resulting in a flat face and developmental defects of the extremities Incompatible with life.

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8
Q

Potter Sequence

A

aka Oligohydramnios sequence.

  • Typically resulting from renal agenesis but can be associated with other disease that ultimately result in lack of kidneys.
  • Amniotic fluid (AF) is essentially the filtrate coming from the kidney (baby is basically floating in its own urine)
  • Without kidneys, there will be little AF == oligohydramnios.
  • Without the cushioning of AF then the baby will be pressed up against the mother’s uterus resulting in a flat face and developmental defects of the extremities
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9
Q

Dysplastic kidney

A

noninherited, congenital malformation of the renal parenchyma characterized by cysts and abnormal tissue (ie cartilage)

Usually unilateral, but can be bilateral.

When bilateral, need to distinguish from PKD (polycystic kidney disease)

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10
Q

A pregnant mother with diagnosed with dysplastic kidney asks what is the chance that her child will have it? Is there anything she can do to prevent or lower the likelihood?

A

Very little risk. Dysplastic kidney is non-inheritable and carries little risk onto the fetus. The chance that the baby develops it is the same as anyone else

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11
Q

Polycystic kidney disease (PKD)

A

Inherited defect leading to bilateral enlarged kidneys with cysts in the renal cortex and medulla

Presents as 2 forms: autosomal recessive and autosomal dominant

  • Autosomal recessive
    • previously called juvenille PKD because it mainly affects infants
    • presents as worsening renal failure and HTN
    • newborns may present with Potter sequence
    • associated with congenital hepatic fibrosis (results in portal HTN) and hepatic cysts
  • Autosomal dominant
    • due to mutation in APKD1 or APKD2 gene
    • cysts develop over time (and will present later in life)
    • associated with berry aneurysms, hepatic cysts and mitral valve prolapse
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12
Q

PKD - autosomal recessive form

A

High yield: inheritable, enlarged kidneys, always bilateral, renal cortex and medulla involvement

  • previously called juvenille PKD because it mainly affects infants
  • presents as worsening renal failure and HTN
  • newborns may present with Potter sequence
  • associated with congenital hepatic fibrosis (results in portal HTN) and hepatic cysts
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13
Q

PKD - autosomal recessive form (major presentation)

A
  • Cysts in kidney –> enlarged kidneys
  • Cysts in liver –> hepatic fibrosis –> portal HTN
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14
Q

PKD - autosomal dominant form (major presentation)

A
  • Cysts in kidney –> enlarged kidneys
  • Cysts in liver –> hepatic fibrosis –> portal HTN
  • Cysts in brain === (not really cysts, but look like it) Berry aneuryms
  • mitral valve prolapse
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15
Q

PKD - autosomal dominant form (mutation)

A

APKD1 or APKD2

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16
Q

PKD - autosomal dominant form (when and how does it normally present?)

A

presents in adults as HTN due to increased renin, hematuria and worsening renal failure

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17
Q

Medullary cystic kidney disease

A
  • Inherited (autosomal dominant) defect leading to cysts in the medullary collecting ducts
  • Parenchymal fibrosis results in shrunken kidneys and worsening renal failure
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18
Q

How do you distinguish between medullary cystic kidney disease and PKD?

A

MCKD – shrunken kidneys. Involve medullary collecting ducts

PKD – enlarged kidneys. Involve both medullary and cortical portions of kidney

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19
Q

Hallmark of acute renal failure

A

azotemia (increased BUN and creatinine)

  • “azot” - nitrogen
  • “emia” - in the blood
  • often occurs with oliguria
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20
Q

Divisions of acute renal failure (3)

A

pre-renal, postrenal and intrarenal

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21
Q

Prerenal azotemia - cause?

A

Decreased blood flow to kidneys (almost always due to cardiac failure)

Commonly causes acute renal failure

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22
Q

Prerenal azotemia - clinical features

A
  • Decreased GFR
  • azotemia
  • oliguria
  • serum BUN:Cr ratio > 15
  • FENa < 1% (normal)
  • Urine osmolarity > 500mOsm/kg (normal)
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23
Q

Prerenal azotemia - pathogenesis

A

decreased RBF = decreased GFR –> more pooling of blood in the renal tubules (slower travel speed) –> more re-absorption of urea in the proximal tubules

Creatinine is not re-absorbed (only secreted).

More uptake of urea than creatinine will result in a ratio >15.

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24
Q

Postrenal azotemia - cause

A

obstruction of urinary tract downstream from the kidney (ie ureters)

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25
Q

Postrenal azotemia - clinical features

A
  • Decreased GFR
  • azotemia
  • oliguria
  • serum BUN:Cr ratio > 15
  • FENa and urine osmolarity depends on the stage of obstruction (and length of time)
    • normal during early stages and malfunctional later on
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26
Q

Postrenal azotemia - early stages

A
  • Decreased GFR
  • azotemia
  • oliguria
  • serum BUN:Cr ratio > 15 (increased pressure pushes urea back into the blood)
  • Renal tubular function still intact and will result in a normal FENa (<1%) and urine osmolarity (>500mOsm/kg)
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27
Q

Postrenal azotemia - late stages

A

Renal tubular function no longer working. Basically long term increased backup (HTN) of renal tubules will damage the lining of the tubules and cause damage. No longer absorbing urea because of this damage.

  • BUN:Cr < 15
  • FENa > 2% (inability to reabsorb sodium)
  • urine osmolarity < 500mOsm/kg (inability to concentrate urine)
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28
Q

Acute tubular necrosis

A

Injury and necrosis of tubular epithelial cells

most common cause of acute renal failure (intrarenal azotemia)

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29
Q

Most common cause of acute renal failure

A

Intrarenal azotemia (aka acute tubular necrosis)

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30
Q

Acute tubular necrosis - pathogenesis

A
  1. necrotic cells plug tubules: obstruction decreases GFR
  2. Increased pressure in the renal tubule (due to obstruction)
  3. decreased filtration (essentially b/c the pressure pushes all the solutes back into the blood)
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31
Q

Acute tubular necrosis - clinical features

A

Depends on the stage (early or late) and the mechanism.

Typically associated with

  • oliguria with brown, granular casts
  • Elevated BUN and creatinine
  • Hyperkalemia (due to decreased renal excretion) with metabolic acidosis
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32
Q

Differences between the early and late stages of postrenal azotemia

A
  • BUN:Cr ratio > 15 in early but < 15 in later stages when the tubules are damaged and can’t reabsorb urea any longer
  • FENa > 2% in later stages (dysfunctional tubular epithelium)
  • Urine osmolarity normal in early, but lowered in late phase when there is an inability to concentrate urine due to tubular destruction
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33
Q

Acute tubular necrosis - etiologies (2)

A
  1. Ischemic – often preceded by prerenal azotemia (decreased blood flow –> ischemia)
  2. Nephrotoxic – toxic agents result in necrosis of tubules
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34
Q

What segments of renal tubules are affected in ischemic ATN?

A

proximal tubule and medullary segment of the thick ascending limb are particularly susceptible to ischemic damage

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35
Q

What often precedes ischemic ATN (acute tubular necrosis)?

A

prerenal azotemia

Decreased blood flow that causes prerenal azotemia will ultimately cause ischemia if every supply is deprived (renal system requires a lot since it always has to function; demand is quite high)

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36
Q

What are some common causes of nephrotoxic ATN (acute tubular necrosis)?

A
  • aminoglycosides (most common)
  • heavy metals (ie lead)
  • myoglobinuria (ie from crush injury to muscle)
  • ethylene glycol ( associated with oxalate crystals in urine)
  • radiocontrast dye
  • urate (tumor lysis syndrome)
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37
Q

How does tumor lysis syndrome cause increased levels of urate?

A

Tumor lysis syndrome is what happens when chemotherapy is initially started resulting in the death of a large number of cells (the tumor) causing a large turnover of cells.

The large turnover will activate the purine salvage pathway that ultimately generates uric acid and increase the likelihood of having urate crystals flowing around (that can cause obstruction)

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38
Q

What is used to decrease risk of urate-induced ATN?

A
  • Hydration (dilutes the level of uric acid and decreases likelihood of crystallization)
  • allopurinol (prevents synthesis by inhibition of xanthine oxidation)
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39
Q

Why is there hyperkalemia and metabolic acidosis in ATN (acute tubular necrosis)?

A

Both cause from decreased function of tubular epithelium to secrete potassium (hyperkalemia) and organic acids (metabolic acidosis)

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40
Q

Acute tubular necrosis - prognosis

A
  • Reversible but requires supportive dialysis since electrolyte imbalances can be fatal
  • Oliguria can persist for 2-3 weeks before recovery
    • tubular cells (stable cells) take time to reenter the cell cycle and regenerate
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41
Q

Acute interstitial nephritis

A

Drug-induced hypersensitivity involving the interstitium and tubules resulting in acute renal failure (via intrarenal azotemia)

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42
Q

Acute interstitial nephritis - causes

A

NSAIDs, penicillin, and diuretics

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43
Q

How does NSAIDs affect the renal vasculature?

A

There are 2 mechanisms by which the kidneys can increase blood flow: vasodilation of the afferent arterioles (via prostaglandins) and vasoconstriction of the efferent arterioles (via angiotensin II) NSAIDs inhibits COX which synthesizes prostaglandins which can decrease blood flow to the kidneys

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44
Q

Acute interstitial nephritis - clinical presentation

A
  • Fever and rash (typical of hypersensitivity)
  • oliguria (renal failure)
  • Eosinophils may be seen in urine (hallmark of acute interstitial nephritis)
  • Typically starts weeks after starting a drug and resolves with cessation of drug
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45
Q

Hallmark of Acute interstitial nephritis

A

eosinophils in urine

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46
Q

Acute interstitial nephritis - treatment

A

Remove drug. Usually resolves with cessation of drug

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47
Q

Acute interstitial nephritis - complication (what can it progress into?)

A

May progress into renal papillary necrosis

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48
Q

Renal papillary necrosis

A

Necrosis of the renal papillae

Presents with gross hematuria and flank plain

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49
Q

Renal papillary necrosis - presentation

A

gross hematuria and flank plain

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50
Q

Renal papillary necrosis - causes

A
  1. Chronic analgesic abuse (long-term phenacetin or aspirin use)
  2. Diabetes mellitus
  3. Sickle cell trait or disease
  4. Severe acute pyelonephritis
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51
Q

What are some causes of intrarenal azotemia? (3)

A
  • Acute tubular necrosis (ischemic or nephrotoxic)
  • Acute interstitial nephritis
  • Renal papillary necrosis (may just be a progression of the previous disease)
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52
Q

Nephrotic syndrome

A

Hallmark: Proteinuria (>3.5g/day)

Characterized additionally by:

  • hypoalbuminemia –> pitting edema (due to decreased oncotic pressure)
  • hypogammaglobulinemia –> increased risk of infection
  • hypercoagulable state – due to loss of antithrombin III
  • hyperlipidemia and hypercholesterolemia –> may result in fatty casts in urine
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53
Q

4 characteristics of nephrotic syndrome

A
  1. hypoalbuminemia –> pitting edema (due to decreased oncotic pressure)
  2. hypogammaglobulinemia –> increased risk of infection
  3. hypercoagulable state – due to loss of antithrombin III
  4. hyperlipidemia and hypercholesterolemia –> may result in fatty casts in urine
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54
Q

nephrotic syndrome - why is there a hypercoagulable state?

A

Loss of Antithrombin III

Antithrombin is the inhibitor of thrombin which cleaves fibrinogen to fibrin.

  • Loss of this inhibition will result in a pro-coagulation state
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55
Q

nephrotic syndrome - why is there hyperlipidemia and hypercholesterolemia?

A

Think of it as due to the huge losses in protein in the urine which thins out the blood, the liver tries to compensate by dumping lipids and cholesterol into the blood to make up for the losses (since it can’t make up that much protein)

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56
Q

Nephrotic Syndromes (6)

A

Think of them in pairs

  • Minimal change disease, FSGS (Focal Segmental Glomerulosclerosis)
    • both due to the effacement of the podocytes
  • Membranous nephropathy, membranoproliferative glomerulonephritis
    • both due to immune complex deposition in the membrane (membranous in the epithelial/subepithelial layer, Type 1 in the subendothelial, type 2 within the basement membrane)
  • Diabetes mellitus, systemic amyloidosis
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57
Q

Minimal change disease

A
  • Most common cause of nephrotic syndrome in children
  • Characterized by the effacement of the podocyte foot processes on electron microscopy
    • due to cytokines
    • Negative IF. No immune complex deposits
  • Usually idiopathic but may be associated with Hodgkin lymphoma (where there is an overproduction of cytokines)
  • Normal glomeruli on H&E stain – lipid may be seen in proximal tubule cells
  • Selective proteinuria (loss of albumin, but not immunoglobulin)
  • Excellent response to steroids (damage mediated by cytokines from T cells)
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58
Q

Minimal change disease - treatment and prognosis

A

Steroids – excellent response

ONLY nephrotic syndrome w/ an excellent response to treatment

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59
Q

Minimal change disease - cause

A

Effacement of foot processes due to cytokines (which is why it responds well to treatment)

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60
Q

Minimal change disease - H&E stain

A

Will mostly look normal. Normal glomeruli

Podocytes are damage (effaced/flattened), but you can’t see that unless on EM

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61
Q

Focal Segmental Glomerulosclerosis (FSGS)

A
  • Most common cause of nephrotic syndrome in Hispanics and African Americans
  • Usually idiopathic, but may be associated with HIV, heroin use, and sickle cell disease
  • Characterized by focal (some glomeruli) and segmental (involving only part of the glomerulus) sclerosis on H&E stain
    • Effacement of foot processes on EM
  • No immune complex deposits, negative IF
  • poor response to steroids – progresses to chronic renal failure
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62
Q

Focal Segmental Glomerulosclerosis (FSGS) - causes?

A

Usually idiopathic, but commonly associated with:

  • HIV
  • heroin use
  • sickle cell disease
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63
Q

Focal Segmental Glomerulosclerosis (FSGS) - pathophysiology

A

Effacement of foot processes

Focal (some glomeruli) and segmental (involving only part of the glomerulus) sclerosis on H&E.

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64
Q

Focal Segmental Glomerulosclerosis (FSGS) - prognosis

A

Poor response to steroids.

Progresses to chronic renal failure

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65
Q

You noticed an effacement of foot processes of podocytes in the kidney. How do you distinguish between FSGS and minimal change disease?

A

FSGS responds poorly to steroids. Think of FSGS as the next step in the progression from minimal change disease. The effacement of the podocytes eventually causes sclerosis that progresses to chronic renal failure

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66
Q

If a patient has HIV and then develops nephrotic syndrome, what is the diagnosis?

A

Focal Segmental Glomerulosclerosis (FSGS)

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67
Q

Membranous nephropathy

A
  • Most common cause of nephrotic syndrome in Caucasian adults
  • Usually idiopathic, but may be associated with hepatitis B or C, solid tumors, SLE or drugs (ie NSAIDs and penicillamine)
  • Thick glomerular basement membrane on H&E
  • Characterized by immune complex deposition (granular IF)
    • subepithelial deposits with ‘spike and dome’ appearance on EM
  • Poor response to steroids – progresses to chronic renal failure
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68
Q

Most common cause of death in lupus patients?

A

Renal failure

  • Most commonly due to diffuse proliferative glomerulonephritis (nephritic syndrome)
  • If the patient has nephrotic syndrome – it is membranous nephropathy
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69
Q

Membranous nephropathy - associated diseases

A
  • Hepatitis B or C
  • solid tumors
  • SLE
  • drugs (ie NSAIDs and penicillamine)
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70
Q

Membranous nephropathy - findings on H&E

A

thickened glomerular basement brane

  • immune complex deposition causes hypertrophy/dysplasia and results in thickened membrane
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71
Q
A

Membranous nephropathy

characterized by thickened glomerular BM

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72
Q

Membranous nephropathy - Why is there a thickened glomerular basement membrane?

A

The deposition of the immune complexes (subepithelial) kind of displaces the foot processes so it lays down new basement membrane right ontop of the deposit which thickens the glomerulus (cells do not like to be onto of immune deposits instead of the BM)

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73
Q

Membranous nephropathy - immunofluorescence - what is expected?

A

Granular IF (hard to see unless zoomed in) - granules are the deposits of immune complexes

Subepithelial deposits with “spike and dome” appearance on EM

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74
Q

Membranous nephropathy - prognosis

A

Poor response to steroids – progresses to chronic renal failure

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75
Q

Membranous nephropathy - where are the immune deposits?

A

Subepithelial (in the layer between the basement membrane and the podocyte foot processes)

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76
Q

Membranoproliferative glomerulonephritis

A
  • Thick glomerular BM on H&E often with ‘tram-track’ appearance
  • Characterized by immune complex deposition (Granular IF)
  • Divided into two types based on location of deposit
    • Type I – subendothelial
      • associated with HBV and HCV
      • More commonly associated w/ tram-track appearance than type II
    • Type II – intramembranous
      • associated with C3 nephritic factor (autoantibody that stabilizes C3 convertase, leading to overactivation of complement, inflammation and low levels of circulating C3)
  • Poor response to steroids – progresses to chronic renal failure
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77
Q

Membranoproliferative glomerulonephritis - subdivisions (2)

A

Type I – subendothelial immune complex depositions

  • associated with HBV and HCV
  • More commonly associated w/ tram-track appearance than type II

Type II – intramembranous immune complex depositions

  • associated with C3 nephritic factor (autoantibody that stabilizes C3 convertase, leading to overactivation of complement, inflmmation and low levels of circulating C3)
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78
Q

Membranoproliferative glomerulonephritis - why is there a tram-track appearance?

A

The deposition of immune complexes stimulates the “proliferation” of mesangial cells to essentially cut through the immune deposit splitting it into 2 halves and creating the ‘tram-track’ appearance

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79
Q

Membranoproliferative glomerulonephritis - what is different between the subdivisons (type 1 vs 2)?

A

Type 1 - has more to associations with tram-track appearance and are subendothelial deposits

Type 2 - intramembranous deposit (within the basement membrane). Associated with C3 convertase overactivation

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80
Q

Membranoproliferative glomerulonephritis - prognosis

A

Poor response to steroids – progresses to chronic renal failure

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81
Q

What does C3 convertase do? What does it have to do with the renal pathophysiology?

A

Normally activates C3 to create C3a and C3b.

Normally only activated for a short period of time. However, in Membranoproliferative glomerulonephritis type II, it is stabilized by C3 nephritic factor, an auto antibody that stabilizes C3 convertase leading to the overactiation of complement, inflammation and low levels of circulating C3

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82
Q

In membranoproliferative glomerulonephritis, why is there low levels of C3?

A

C3 converatase is an enzyme that activates C3 to create C3a and C3b.

Normally C3 converatase is only activated for a short period of time. However, in Membranoproliferative glomerulonephritis type II, it is stabilized by C3 nephritic factor, an auto antibody that stabilizes C3 convertase leading to the overactiation of complement, inflammation and low levels of circulating C3

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83
Q

associated diseases of type I membranoproliferative glomerulonephritis?

A

Hep B or C (HBV or HCV)

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84
Q

What is the difference between membranous nephropathy and membranoproliferative glomerulonephritis?

A

Membranous nephropathy – immune deposits in subepithelial layer (between BM and foot processes)

Membranoproliferative glomerulonephritis

  • Type I - subendothelial
  • Type II - intramembranous
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85
Q

How does diabetes mellitus affect renal pathophysiology?

A
  • High serum glucose leads to nonenzymatic glycosylation (first change to occur in the kidney in the diabetes) of the vascular baement membrane resulting in hyaline arteriolosclerosis
  • Preferentially affects the efferent arterioles (results in increased glomerular filtration pressure)
    • increased hydrostatic pressure results in microalbuminuria (essentially pushes it out)
  • Eventually progresses to nephrotic syndrome
    • characterized by sclerosis of the mesangium w/ formation of Kimmelstiel-Wilson nodules
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86
Q

First physiological change to happen to the kidney in diabetes

A

High serum glucose leads to nonenzymatic glycosylation of the vascular baement membrane resulting in hyaline arteriolosclerosis

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87
Q

What occurs after nonenzymatic glycosylation of basement membrane of kidney vasculature? and where does it occur?

A

Hyaline arteriolosclerosis

Preferentially affects the efferent arterioles (results in increased glomerular filtration pressure)

  • increased hydrostatic pressure results in microalbuminuria (essentially pushes it out)
88
Q

Treatment for diabetes mellitus associated renal problems? how does it work?

A

ACE inhibitors slow progression of hyperfiltration-induced damage (helps to vasodilate the efferent arteriole so the it can minimize the narrowing that occurred due to hylaine arteriolosclerosis

89
Q

Nephrotic syndrome due to diabetes mellitus - what is the major characteristic?

A

Sclerosis of the mesangium w/ formation of Kimmelstiel-Wilson nodules

90
Q
A

Kimmelstiel-Wilson nodules

Found in nephrotic syndrome due to diabetes mellitus

  • characterized by sclerosis of the mesangium and the formation of these bodies
91
Q

What commonly involved organ in systemic amyloidosis?

A

Kidney

92
Q

Systemic amyloidosis affecting the liver

A

Amyloid deposits in the mesangium, resulting in nephrotic syndrome

Characterized by apple-green birefringence under polarized light after staining w/ Congo Red

93
Q

Biopsy of kidney finds apple-green birefringence under polarized light after staining w/ Congo Red

What is the diagnosis?

A

Systemic amyloidosis

94
Q

Nephrotic syndrome most common in kids/children?

A

minimal change disease

95
Q

Nephrotic syndrome most common in hispanics and african americans?

A

Focal segmental glomerulosclerosis

96
Q

Nephrotic syndrome most common in Caucasian adults?

A

Membranous nephropathy

97
Q

Nephritic syndrome

A
  1. Limited proteinuria (<3.5g/day)
  2. oliguria and azotemia
  3. salt retention –> periorbital edema and HTN
    • perioribital b/c of the loose CT that is present there so tends to show first
  4. RBC casts and dysmorphic RBCs in urine
98
Q

Nephritic syndrome - biopsy findings

A

Hypercellular, inflamed glomeruli

  • Immune-complex deposition activates complement; C5a attracts neutrophils which mediate damage and the inflammatory response
99
Q

Nephritic syndrome - most common types (4)

A
  1. Poststreptococcal glomerulonephritis
  2. Rapidly progressive glomerulonephritis
  3. IgA nephropathy (Berger Disease)
  4. Alport Syndrome
100
Q

Poststreptococcal Glomerulonephritis (PSGN)

A
  • Nephritic syndrome that arises after group A ß-hemolytic streptococcal infection of the skin (impetigo) or pharynx
    • occurs with nephritogenic strains (carry the M protein virulence factor)
    • May occur after infection w/ nonstreptococal organisms as well
  • Presents 2-3 weeks after infection as hematuria (cola-colored urine), oliguria, HTN and periorbital edema
    • Usually seen in children but may occur in adults
  • Mediated by subepithelial ‘humps’ on EM
  • Treatment is supportive
101
Q

What makes a bacterial strain nephritogenic?

A

If they carry the M protein virulence factor usually present in the Group A ß-hemolytic streptococci.

102
Q

Poststreptococcal Glomerulonephritis (PSGN) - presentation

A

Presents 2-3 weeks after infection with:

  • hematuria (cola-colored urine)
  • oliguria
  • HTN
  • periorbital edema
103
Q

Poststreptococcal Glomerulonephritis (PSGN) - pathogenesis

A

Immune complex deposition as a response to the infection.

Deposits start out as subendothelial deposits that continue to move out and dissipate (disease is self-limiting). They do however congregate/pileup in the subepithelial layer creating the subepithelial “humps” that is characteristic of this disease

104
Q

Poststreptococcal Glomerulonephritis (PSGN) - treatment

A

Supportive. The immune deposits eventually move themselves out of the system.

  • Children rarely progress to renal failure (1%)
  • Some adults (25%) develop rapidly progressive glomerulonephritis
105
Q

Poststreptococcal Glomerulonephritis (PSGN) - hallmark of the disease

A

subepithelial ‘humps’ – from the progressive outward movement of the immune deposits that start from the subendothelial deposit and move outward piling up in the subendothelial cell layer to create humps

106
Q

Rapidly progressive glomerulonephritis (RPGN)

A

Nephritic syndrome that progresses to renal failure in weeks to months

Characterized by crescents in Bowman space on H&E stain – comprised of fibrin and macrophages

Clinical picture and IF help resolve etiology

107
Q

Rapidly progressive glomerulonephritis - hallmark

A

Crescents in Bowman space comprised of fibrin and macrophages

108
Q

What is a complication in poststreptococcal glomerulonephritis in adults?

A

May progress to rapidly progressive glomerulonephritis (25%) which can result in renal failure in weeks to months

109
Q

Rapidly progressive glomerulonephritis - some causes

A
  • Goodpasture syndrome – causes a linear IF pattern
  • PSGN or diffuse proliferative glomerulonephritis
  • Wegener granulomatosis, Churg-Strauss syndrome, microscopic polyangiitis
110
Q

Rapidly progressive glomerulonephritis - IF findings

A
  1. Linear (anti-basement membrane antibody) –> goodpasture syndrome
  2. Granular (immune complex deposition) –> PSGN (most common) or diffuse proliferative glomerulonephritis
  3. Negative IF (pauci-immune) –> any of the small vessel vasculities
111
Q

If a patient was found to have rapdily progressive glomerulonephritis. The immunofluorescence (IF) comes back with a linear pattern. What does it mean? What is the diagnosis and why?

A

Linear pattern means it is an anti-basement membrane antibody.

  • Ab against collagen in glomerular and alveolar basement membranes
    • BOTH lung and renal involvement –> hematuria and hemoptysis
  • Classically seen in young, adult males

Disease/Diagnosis: Goodpasture syndrome

112
Q

If a patient was found to have rapdily progressive glomerulonephritis. The immunofluorescence (IF) comes back with a granular IF pattern. What does it mean? What is the diagnosis and why?

A
  • Granular IF means immune complex deposition.
  • This is most commonly due to poststreptococcal glomerulonephritis (PSGN) – which is characterized by immune complex deposits.
  • Can also be associated with diffuse proliferative glomerulonephritis
    • ​due to diffuse antigen-antibody complex deposition, usually sub-endothelial. Most common type of renal disease in SLE
113
Q

Diffuse Proliferative glomerulonephritis

A

​due to diffuse antigen-antibody complex deposition, usually sub-endothelial. Most common type of renal disease in SLE

114
Q

If a patient was found to have rapdily progressive glomerulonephritis. The immunofluorescence (IF) comes back negative. What does it mean? What is the diagnosis and why?

A
  • Negative IF aka pauci-immune.
  • Associated with any of the small vessel vasculitis (Wegeners, microscopic polyangiitis and Churg-Strauss syndrome)
    • Wegener granulomatosis is associated with c-ANCA
    • Microscopic angiitis associated with p-ANCA
    • Churg-Strauss Syndrome associated with p-ANCA. However it can be distinguished from microscopic b/c of granulomatous inflammation, eosinophilia and asthma.
115
Q

Similarities and differences between Churg-Strauss syndrome and microscopic polyangiitis

A

Similarities: both affect small vessels and associated with p-ANCA

Differences: only Churg-Strauss is associated with granulomatous inflammation, eosinophilia and asthma

116
Q

IgA nephropathy (Berger Disease)

A
  • IgA immune complex deposition in mesangium of glomeruli – most common nephropathy worldwide
  • presents during childhood as episodic gross or microscopic hematuria with RBC casts, usually following mucosal infections (ie gastroenteritis)
    • response of a mucosal infection is to produce a lot of IgA
  • May slowly progress to renal failure
117
Q

What is the mesangium in terms of renal structure?

A

In the glomerulus of the kidney, the mesangium is a structure associated with the capillaries. It is continuous with the smooth muscles of the arterioles. It is outside the capillary lumen, but surrounded by capillaries. It is in the middle (meso) between the capillaries (angis). It is contained by the basement membrane, which surrounds both the capillaries and the mesangium.

In the picture, it is (5b) – the pink stuff inbetween all the capillaries

118
Q

Most common nephropathy worldwide

A

IgA nephropathy (Berger Disease)

119
Q

IgA Nephropathy - when does it normally present? in what population?

A

Typically presents in childhood following mucosal infections (such as gastroenteritis)

IgA production is increased during infection (increased chance of deposition)

120
Q

Alport syndrome

A

Inherited defect in Type IV collagen – most commonly X-linked

Results in thinning and splitting of the glomerular BM

Presents as isolated hematuria, sensory hearing loss and ocular disturbances

  • all due to the splitting of BM in each symptom’s respective areas
121
Q

What disease is associated with an inherited defect in type IV collagen?

A

Alport syndrome – most commonly X-linked

122
Q

Alport syndrome – pathogenesis

A

Defect in type IV collagen (the collagen responsible for basement membranes)

Results in thinning and splitting of basement membranes, particularly in the kidney –> isolated hematuria

However this occurs everywhere and can frequently cause sensory hearing loss and ocular disturbances.

123
Q

Urinary track infection - possible sites of infection

A

urethra, bladder or kidney

124
Q

Urinary track infection - most common cause? Who is more at risk and why?

A

Due to ascending infection. Women are more at risk due to shorter urethra (shorter distance of travel)

125
Q

Why are women more at risk for UTIs?

A

Shorter urethra makes it shorter distance for infection to travel to reach destination

126
Q

Cystitis

A

infection of the bladder

127
Q

Cystitis - clinical presentation

A
  • Dysuria
  • urinary frequency
  • urgency
  • suprapubic pain

Systemic signs (ie fever) usually absent

128
Q

Cystitis - laboratory findings

A
  • Urinalysis - cloudy urine w/ >10 WBCs/high power field
  • Dipstick
    • positive leukocyte esterase (due to pyuria)
    • positive nitrites (bacteria convert nitrates to nitrites)
  • Culture - greater than 100,000 CFUs (gold standard)
129
Q

What is the gold standard for labs for identifying cystitis?

A

> 100,000 CFUs

130
Q

Cystitis - common causes (etiologies)

A
  1. E. coli (80%)
  2. Staphylococcus saprophyticus - increased incidence in young, sexually active women
  3. Klebsiella pneumoniae
  4. Proteus mirabilis - causes alkaline urine with ammonia scent
  5. Enterococcus faecalis
131
Q

Sterile pyuria

A

Presence of > 10 WBCs/hpf and leukocyte esterase

w/ negative urine culture (gold standard)

132
Q

If a patient is found with sterile pyuria, what bugs come to mind?

A

Chlamydia trachomatis or Neisseria gonorrhoeae

133
Q

Pyelonephritis

A

Infection of the kidney

Usually due to ascending infection. Increased risk with vesicoureteral reflux

134
Q

Pyelonephritis - cause?

A

Usually due to ascending infection. Increased risk with vesicoureteral reflux

135
Q

Pyelonephritis - presentation

A
  • Fever
  • flank pain (sensitization of nerves of the capsule due to inflammation)
  • WBC casts (reflux of not just the bacteria but also the inflammatory cells)
  • Leukocytosis
  • Symptoms of cystitis
136
Q

Pyelonephritis - why is there flank pain?

A

Inflammation causes sensitization of the nerves of the renal capsule

137
Q

Pyelonephritis - most common pathogens

A
  • E. coli (90%)
  • Enterococcus faecalis
  • Klebsiella species
138
Q

Chronic Pyelonephritis

A
  • Interstitial fibrosis and atrophy of tubules due to multiple bouts of acute pyelonephritis
  • Due to vesicoureteral reflux (children) or obstructure (ie BPH or cervical carcinoma in adults)
  • Leads to cortical scarring with blunted calyces – scarring at upper and lower poles is characteristic of vesicoureteral reflux
139
Q

Chronic Pyelonephritis - most common cause in children?

A

Vesicoureteral reflux

140
Q

Chronic Pyelonephritis - most common cause in adults?

A

obstruction (ie BPH or cervical carcinoma)

141
Q

Chronic Pyelonephritis - what kind of scarring can you expect to see?

A

Cortical scarring with blunted calyces

Scarring at upper and lower poles is characteristic of vesicoureteral reflux

142
Q

Chronic Pyelonephritis - histological findings

A

Atrophic tubules containing eosinophilic proteinaceous material resembling thyroid follicles (‘thyroidization’ of the kidney)

Waxy casts may be seen in urine

143
Q

What is meant by ‘thyroidization’ of the kidney?

A

Atrophic tubules containing eosinophilic proteinaceous material that resemble thyroid follicles

Waxy casts may be seen in urine

144
Q

Nephrolithiasis

A
  • Precipitation of a urinary solute as a stone
  • Risk factors incude high concentration of solute in urinary filtrate and/or low urine volume
  • Presents as colicky pain with hematuria and unilateral flank tenderness
    • stone is usually passed within hours, if not, surgical intervention may be required
145
Q

Nephrolithiasis - risk factors

A

High concentration solute in urine

Low urine volume

146
Q

Nephrolithiasis - presentation

A

Colicky pain with hematuria and unilateral flank tenderness

Stone should pass within hours (otherwise surgery may be needed)

147
Q

Nephrolithiasis - types (4)

A
  1. Calcium oxalate and/or calcium phosphate
  2. Ammonium magnesium phosphate
  3. Uric acid
  4. Cystine
148
Q

Most common cause of calcium oxalate and/or calcium phosphate nephrolithiasis

A

Idiopathic hypercalciuria

Counter-intuitive – the most common cause is not hypercalcemia but it needs to be excluded

149
Q

calcium oxalate and/or calcium phosphate nephrolithiasis - what disease is associated with this? Why?

A

Crohn’s disease – small bowel destruction causes increased reabsorption of oxalate in the large intestines

This increase in oxalate binds calcium and ends up in the kidney where the increased concentration makes it more likely to precipitate.

150
Q

calcium oxalate and/or calcium phosphate nephrolithiasis - treatment and why?

A

hydrochlorothiazide

Causes calcium reabsorption to reduce the concentration of calcium and chance of precipitation

151
Q

Most common type of nephrolithiasis

A

calcium oxalate and/or calcium phosphate nephrolithiasis

152
Q

Ammonium magnesium phosphate nephrolithiasis - cause?

A

Most common cause is infection with urease-positive organisms (ie Proteus vulgaris or Klebsiella) –> creates an alkaline urine that leads to formation of stone (favors precipitation)

153
Q

Ammonium magnesium phosphate nephrolithiasis - complication?

A

Classically results in staghorn calculi in renal calyces, which act as a nidus for UTIs

154
Q

Ammonium magnesium phosphate nephrolithiasis - treatment

A

Surgical removal of staghorn calculi (due to size) and eradication of the pathogen (to prevent recurrence)

155
Q

Uric acid nephrolithiasis

A
  • Third most common stone
  • Radiolucent (can’t see on xray)
  • Risk factors: hot and arid climates low urine volume, acidic pH
  • Most common stone seen in patients with gout; hyperuricemia (ie in leukemia or myeloproliferative disorders) increases risk
156
Q

Uric acid nephrolithiasis - risk factors

A

hot and arid climates

low urine volume

acidic pH

157
Q

What effect does acidic pH have on nephrolithiasis?

A

acidic pH favors precipitation and increases the risk of stone formation

158
Q

What is common and different between the types of stones found on xray?

A

Calcium, ammonium magnesium phosphate and cystine nephrolithiasis are radiopaque or radiodense

Uric acid nephrolithasis is radiolucent (hard to identify on xray)

159
Q

Uric acid nephrolithasis - treatment

A

hydration (dilution of urate) and/or alkalinization of urine (w/ potassium bicarbonate)

Allopurinol additionally added in patients with gout

160
Q

Cystine nephrolithiasis

A

Rare cause most commonly seen in children

Associated with cystinuria (a genetic defect of tubules that results in decreased reabsorption of cysteine)

May form staghorn calculi

161
Q

Cystine nephrolithiasis - treatment

A

Hydration and alkalinzation

162
Q

What types of nephrolithiasis can result in staghorn calculi?

A

Most common in ammonium magnesium phosphate nephrolithiasis

Can also be seen in cystine nephrolithiasis

163
Q

Chronic renal failure

A

aka end-stage kidney failure

May result from glomerular, tubular, inflammatory, or vascular insults

Most common cause: diabetes mellitus, HTN and glomerular disease

164
Q

Chronic renal failure - most common causes

A

diabetes mellitus

HTN

glomerular disease

165
Q

Chronic renal failure - clinical features

A
  1. Uremia – can result in nausea, anorexia, pericarditis, platelet dysfunction, encephalopathy w/ asterixis and deposition of urea cyrstals in skin
  2. salt and water retention with resulting HTN
  3. hyperkalemia w/ metabolic acidosis (decreased secretion of K+ and organic acids)
  4. Anemia due to decreased EPO production by renal peritubular interstitial cells
  5. hyperphosphatemia and hypocalcemia – due to decreased 1-alpha-hydroxylation of vitamin D (activation step) by proximal renal tubule cells
  6. renal osteodystrophy (osteitis fibrosa cystica, osteomalacia, osteoporosis)
166
Q

Clinical features/complications of uremia

A

Increased nitrogenous waste products in blood (azotemia) result in:

  • nausea
  • anorexia
  • pericarditis
  • platelet dysfunction
  • encephalopathy w/ asterixis
  • deposition of urea crystals in skin
167
Q

Why is there platelet dysfunction in uremia?

A

Nitrogen inhibits both platelet adhesion and aggregation

168
Q

Where and what are responsible for production of erythropoietin (EPO)?

A

Production by renal peritubular interstitial cells

169
Q

Why is there hypocalcemia in chronic renal failure?

A
  1. decreased activation of vitamin D (decreased 1-alpha-hydroxylation by proximal renal tubule cells) –> decreased Ca2+ absorption
  2. hyperphosphatemia –> phosphate will bind Ca2+ so there will be less free calcium
170
Q

Renal osteodystrophy

A

Associated with chronic renal failure due to secondary hyperparathyroidism. 3 key features:

  1. Osteitis fibrosa cystica
    1. decreased calcium levels causes increased PTH secretions that causes bone resorption –> burnout of bone –> fibrosis and formation of cysts (empty due to increased osteoclast activity)
  2. Osteomalacia – can’t mineralize properly due to decreased calcium and vitamin D levels
  3. Osteoporosis – leeching calcium from bones (besides the PTH effect due to low Ca levels) as a means to buffer the metabolic acidosis due to decreased organic acid secretion
171
Q

Chronic renal failure - treatment

A

Dialysis or renal transplant

172
Q

Chronic renal failure - do cysts develop? If so, when?

A

Cysts often develop within shrunken end-stage kidneys during dialysis increasing risk for renal cell carcinoma

173
Q

How to distinguish PKD from chronic renal failure? Especially when both diseases have cyst development?

A

In chronic failure, cysts develop within shrunken end-stage kidneys

PKD has enlarged kidneys.

174
Q

Angiomyolipoma

A

Hamartoma (resembles organ of origin) comprised of blood vessels, smooth muscle and adipose tissue

Increased frequency in tuberous sclerosis

175
Q

What disease is angiomyolipoma associated with?

A

Increased frequency in tuberous sclerosis

176
Q

tuberous sclerosis

A
  • Autosomal dominant genetic disease that causes benign tumors to grown in the brain, kidneys, heart, eyes, kidney, skin and lungs
  • Associated with the lack of TSC1 or TSC1 which code for hamartin and tuberin (tumor growth suppressors)
177
Q

Renal cell carcinoma

A
  • Malignant epithelial tumor arising from kidney tubules
  • Presents with a triad of symptoms: hematuria, palpable mass, and flank pain
    • all 3 symptoms rarely occur together (<10%). Hematuria is most common
    • Fever, weight loss, or paraneoplastic syndrome (EPO, renin, PTHrP or ACTH) may also be present
    • Sometimes include a left sided varicocele (scrotum varicose veins)
  • Associated with loss of VHL tumor suppressor gene
178
Q

Renal cell carcinoma - classic triad of symptoms

A
  1. hematuria
  2. palpable mass
  3. flank pain

Rarely occur together (<10%)

Hematuria is most common presenting symptom

179
Q

Renal cell carcinoma - most common presenting symptom

A

hematuria

180
Q

Renal cell carcinoma - Symptoms

A
  • Triad: hematuria, palpable mass, flank pain
  • Fever, weight loss
  • paraneoplastic syndrome (EPO, renin, PTHrP, or ACTH)
  • left sided varicocele (scrotum varicose veins)
    • carcinoma blocks drainage of the left spermatic vein
181
Q

Paraneoplastic syndromes associated with renal cell carcinoma (4). What results from these syndromes?

A
  1. EPO (job of kidney) –> reactive polycythemia
  2. Renin (job of kidney) –> HTN
  3. PTHrP –> hypercalcemia
  4. ACTH –> Cushings syndrome
182
Q

Cushings syndrome

A

aka hypercortisolism

Characterized by:

  • Increased glucagon activation –> increased gluconeogenesis
    • aberrant gluconeogenesis causes the breakdown of muscle to generate this glucose –> muscle weakness
  • Excess glucose in the blood
    • glucose is absorbed by all cells
      • via insulin dependent maner:
        • fatty deposits around face and upper back
        • fat loss from arms and legs
        • weight gain around midsection
      • via non-insulin dependent manner: (ie neurons)
        • neuropathy (glucose in neurons causes metabolic toxicity)
        • Cataracts (via cells of the lens)
        • blindness (via pericytes of the retina)
  • Immune suppression (inhibition of phospholipase A2, IL2 and histamine release)
  • Osteoporosis (via inhibition of osteoblasts)
  • abdominal striae (via collagen synthesis inhibition)
183
Q

How does renal cell carcinoma result in a left-sided varicocele? Why only the left side?

A

Left spermatic vein drains into the left renal vein which then drains into the IVC. Carcinoma blocks drainage of the left spermatic vein leading to a varicocele (scrotum varicose veins)

Right side drains directly into IVC

184
Q

Spermatic vein drainage

A

Left side –> renal vein –> IVC

right side –> IVC

Left side is more prone to varicocele if there is a block in the renal vein such as in renal cell carcinoma

185
Q

Renal cell carcinoma - gross anatomical presentation

A

yellow mass

186
Q

Renal cell carcinoma - histology

A

most common variant exhibits a clear cytoplasm (cear cell type)

187
Q

Renal cell carcinoma - gene involved? pathogenesis?

A

Involves loss of VHL (3p) tumor suppressor gene

Leads to increased IGF-1 (promotes growth) and increased HIF transcription factor (increases VEGF and PDGF) resulting in excessive growth

188
Q

Renal cell carcinoma - tumor types

A
  • Sporadic or hereditary
  • Sporadic
    • arise in adult males (average age 60)
    • Single tumor in the upper pole of the kidney
    • Major risk factor is cigarette smoke
  • Hereditary
    • arise in young adults
    • often bilateral
    • associated Von HIppel-Lindau disease (autosomal dominant disorder due to inactivation of VHL gene)
      • results in increased risk for hemangioblastoma of the cerebellum and renal cell carcincoma
189
Q

Renal cell carcinoma - sporadic form

A
  • arise in adult males (average age 60)
  • Single tumor in the upper pole of the kidney
  • Major risk factor is cigarette smoke
190
Q

renal cell carcinoma hereditary type

A
  • arise in young adults
  • often bilateral
  • associated Von Hippel-Lindau disease (autosomal dominant disorder due to inactivation of VHL gene)
    • results in increased risk for hemangioblastoma of the cerebellum and renal cell carcincoma
191
Q

What disease is renal cell carcinoma associated with?

A

associated Von Hippel-Lindau disease (autosomal dominant disorder due to inactivation of VHL gene)

The hereditary form is most commonly associated

192
Q

Renal cell carcinoma staging

A

T - based on size and involvement of the renal vein (occurs commonly and increases risk of hematogenous spread to the lungs and bone)

N - spread to retroperitoneal LN

193
Q

Renal cell carcinoma - major risk factor for sporadic tumors?

A

Cigarette smoke

194
Q

Renal cell carcinoma - what vein does it most commonly involve?

A

Love to go the renal vein –> hematogenous spread to lungs and bone

195
Q

Renal cell carcinoma - what lymph nodes does it like to spread to?

A

retroperitoneal LN

196
Q

Wilms tumor

A

Malignant tumor comprised of:

  • blastema (immature kidney mesenchyme)
  • primitive glomeruli and tubules
  • stromal cells

Most common malignant renal tumor in children – average age is 3 years

197
Q

Most common malignant renal tumor in children

A

Wilms Tumor – average age is 3

198
Q

Wilms Tumor - presentation

A

Unilateral flank mass with hematuria and HTN (due to renin secretion)

199
Q

Syndromes that include Wilm’s tumor (3)

A
  1. WAGR – Wilms tumor, Aniridia, Genital abnormalities, and mental & motor Retardation
    • associated w/ deletion of WT1 tumor suppressor gene
  2. Denys-Drash syndrome – Wilms tumor, progressive renal (glomerular) disease and male pseudohermaphroditism
    • associated w/ mutations of WT1
  3. Beckwith-Wiedemann syndrome – Wilms tumor, neonatal hypoglycemia, muscular hemihypertrophy, and organomegaly (including tongue)
    • associated w/ mutations in WT2 gene cluster (imprinted genes at 11p15.5) particularly IGF-2
200
Q

WAGR Syndrome

A
  • Wilms tumor
  • Aniridia (absence of iris)
  • Genital abnormalities
  • mental & motor Retardation

associated w/ deletion of WT1 tumor suppressor gene

201
Q

Denys-Drash syndrome

A
  • Wilms tumor
  • progressive renal (glomerular) disease
  • male pseudohermaphroditism

associated w/ mutations of WT1

202
Q

Beckwith-Wiedemann syndrome

A
  • Wilms tumor
  • neonatal hypoglycemia
  • muscular hemihypertrophy
  • organomegaly (including tongue)

associated w/ mutations in WT2 gene cluster (imprinted genes at 11p15.5) particularly IGF-2

203
Q

Lower urinary tract - what structures does it include? (anatomy)

A
  • renal pelvis
  • ureter
  • bladder
  • urethra
204
Q

Lower urinary tract carcinomas (3)

A
  1. Urothelial (transitional cell) carcinoma
  2. Squamous cell carcinoma
  3. adenocarcinoma
205
Q

Most common type of urinary tract cancer

A

Urothelial (transitional cell) carcinoma – usually arises in bladder

206
Q

Urothelial (transitional cell) carcinoma - risk factors?

A

Major risk factor: cigarette smoke

Other risk factors:

  • naphthylamine (found in cigarette smoke)
  • azo dyes (for coloring such as hair)
  • long-term cyclophosphamide use
  • phenacetin use (for pain relief)
207
Q

Urothelial (transitional cell) carcinoma - population that it mostly affects

A

Generally seen in older adults

208
Q

Urothelial (transitional cell) carcinoma - classic presentation

A

Painless hematuria

209
Q

Urothelial (transitional cell) carcinoma - pathways that it can arise (2)

A
  1. Flat – develops as a high grade flat tumor and then invades
    • associated with early p53 mutations
  2. Papillary – develops as a low-grade papillary tumor that proresses to a high-grade papillary tumor and then invades
    • no associations with p53 mutation
210
Q

What is the ‘field effect’?

What does it have to do with Urothelial (transitional cell) carcinoma ?

A

Field effect refers to when you expose carcinogens to the bladder, you expose it to the whole ‘field’ and hence when you have cancer, it is likely to be multifocal and will like recur (since there can be many different mutations)

211
Q

Urothelial (transitional cell) carcinoma - pathogenesis associated with early p53 mutation

A

Develops initially as a flat high-grade tumor and then invades

212
Q

Progression of a papillary urothelial carcinoma

A

Stars out as a papillary growth (fibrovascular core w/ blood vessel runing through it upon which epithelium is placed).

Develops into a low grade papillary tumor –> progresses to a high grade papillary tumor –> invasion

213
Q

Squamous cell carcinoma of the lower urinary tract

A

Usually involves the bladder.

Normal bladder does NOT have squamous cell epithelium –> requires squamous metaplasia

Risk factors

  • chronic cystitis (older women)
  • Schistosoma haematobium infection (Egyptian male)
  • long-standing nephrolithiasis
214
Q

Risk factors for squamous cell carcinoma of the lower urinary tract

A
  • chronic cystitis (older women)
  • Schistosoma haematobium infection (Egyptian male)
    • inbeds in the bladder wall that causes chronic infection and squamous metaplasia
  • long-standing nephrolithiasis

These all cause chronic inflammation –> which can result in squamous metaplasia (prerequiste to developing this carcinoma)

215
Q

Infection with what bug is associated with squamous cell carcinoma of the lower urinary tract? why?

A

Schistosoma haematobium infection (classically in an Egyptian male)

The bug inbeds in the bladder wall that causes chronic inflammation resulting in squamous metaplasia

216
Q

Adenocarcinoma of the lower urinary tract

A

Malignant proliferation of glands, usually involving the bladder

  • Normal bladder does NOT have glandular epithelium

Arises from:

  • urachal remnant (tumor that develops at the dome of the bladder) – duct that normally connects the fetal bladder w/ the yolk sac. Normally lined with columnar epithelium, but degenerates after birth
  • cystitis glandularis (chronic inflammation that results in columnar metaplasia)
  • exstrophy (congenital failure to form the caudal portion of the anterior abdominal and bladder walls –> exposes the surface of bladder to the outside world –> increased risk for metaplasia)
217
Q

What can cause adenocarinoma of the lower urinary tract?

A

Glandular epithelium not present normally. Requires factors that cause metaplasia or its presence.

  • urachal remnant (tumor that develops at the dome of the bladder) – duct that normally connects the fetal bladder w/ the yolk sac. Normally lined with columnar epithelium, but degenerates after birth
  • cystitis glandularis (chronic inflammation that results in columnar metaplasia)
  • exstrophy (congenital failure to form the caudal portion of the anterior abdominal and bladder walls –> exposes the surface of bladder to the outside world –> increased risk for metaplasia)

Unit 5 (5 decks)

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