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Pathology > Renal > Flashcards

Renal Flashcards

1
Q

Explain how urine is formed and excreted.

A

Urine is formed by ultrafiltration of blood by the kidneys.

nephron = functional unit of the kidney

  • The glomerulus is the specialized capillary bed that allow passage of fluids and soluted from the blood into the lumen of the nephron. The “primary filtrate” is modified during its passage through the nephron. *
  • -approx 1.5 L of urin excreted daily (10% of the blood volume filtered through the glomeruli)*
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2
Q

Describe the principal portions of the nephron and explain how they function.

A

It consists of the glomerulus, convoluted tubules, and collecting ducts.

  • The contents of the primary filtrate are partially resorbed and partially enriched by substances that are secreted into the nephron.*
  • The close positioning of blood vessels allows concentration of urine and selective excretion of minerals and water.*
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3
Q

What is the functional significance of transitional epithelium?

A

it is “waterproof” and can withstand prolonged exposure to urine.

it lines the calices, pelves, ureters, urinary bladder, urethra

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4
Q

Describe the effects of various hormones on the kidney.

A

post. pit. >> ADH >> antidiuresis

atria of heart >> ANH >>

adrenals >> aldosterone

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5
Q

Which hormones and growth factors does the kidney produce?

A

Renin >> raises BP

erythropoietin >> stimulates RBC production

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6
Q

List the most important symptoms of kidney disease.

A

Localized

alterations in volume: oliguria, anuria
alterations in content: proteinuria, glucosuria, hematuria, pyuria

Systemic

infection: fever, shivering, malaise
renal failure: uremia >> CNS changes >> coma/death

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7
Q

How common are renal developmental disorders, and which one of them is the most common?

A

very common

1 in 800 born with 1 kidney

one-sided renal agenesis

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8
Q

Correlate the pathology of autosomal dominant poycystic kidney disease with the clinical features of this disease.

A

inherited Mendelian trait, related to the mutation of polycystin-1* *a cell-to-cell adhesion molecule holding cells together.

  • both kidneys enlarge with cysts
  • tubule obstruction
  • dev. renal failure by 40-50
  • Must distinguish from multicystic renal dysplasia: unilateral*
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9
Q

Classify glomerular diseases.

A
  1. Immunologic
  2. Metabolic
  3. Circulatory
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10
Q

List the most important immunologic glomerular diseases.

A
  • Injury is often mediated by antibodies and classified as Type II (cytotoxic) or Type III (immune complex) hypersensitivity reaction.*
  • Immunoglobulins deposit in the glomeruli and cause inflammation = glomerulonephritis*

*secondary >> tubulointerstitial

- wegener’s granulomatosis

Immunoglobulins deposit in the glomeruli and NO inflammation = glomerulopathies

- **lipoid nephrosis**

- membranous nephropathy

- Berger’s disease

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11
Q

List the most important metabolic glomerulopathies.

A

Caused by systemic metabolic disorders

- diabetes

- amyloidosis

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12
Q

Explain how circulatory disorders affect glomeruli.

A

atherosclerosis: hypoperfusion >> involution and hyalinzation

sudden onset HTN: possible fibrinoid necrosis

shock/DIC: microthrombi

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13
Q

List the four most imporant syndromes related to glomerular diseases.

A
  1. Acute renal failure
  2. Nephritic syndrome
  3. Nephrotic syndrome
  4. Isolated hematuria and/or proteinuria
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14
Q

Compare nephrotic and nephritic syndrome.

A

nephritic syndrome = ususally caused by acute poststreptococcal or postinfectious glomerulonephritis

generalized edema, HTN, hematuria, proteinuria, hypoalbuminemia

nephROtic syndrome = usually caused by lipoid nephrosis (children) or focal glomerulosclerosis + membranous nephropathy + diabetes (adults)

generalized edema, proteinuria, hypoalbuminemia, and hyperlipidemia, lipiduria

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15
Q

Explain the pathogenesis of acute glomerulonephritis and correlate the pathologic and clinical findings in this disease.

A

Antigen-antibody complexes are trapped in glomerular basement membranes >> activate complement and attract inflammatory cells.

Hypercellularity occurs, partly b/c mesangial cells proliferate in response to injury.

Deposits of immune comlexes on the epithelial side of the basement membrane form “humps”.

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16
Q

Explain the pathogenesis of crescentic glomerulonephritis and relate the pathologic and cliical findings in this disease.

A

= severe glomerular injury accompanied by the formation of exudate (marcrophages that have drossed between damaged glomerular capillaries)

Inflammatory cells surround the compressed capillary loops in the form of a crescent moon. Macrophages are gradually replaced by fibroblasts, which secrete collagen >> scarring and complete obliteration of glomeruli.

17
Q

Explain the pathogenesis of membranous nephropathy and relate the pathologic and clinical findings of the disease.

A

Massive deposition of immune complexes >> nephritic syndrome. NO EVIDENCE of INFLAMMATION.

18
Q

What is lipoid nephrosis, and how is it diagnosed?

A

Nephrotic syndrome + hyperlipidemia and lipiduria
**Glomeruli show no changes on light microscopy. **

19
Q

What do most forms of chronic proliferative glomerulonephritis have in common?

A

they all have . . . a chronic course, do not responde to treatment, progress to ESRD.

20
Q

What is the cause of end-stage kidney disease, and how does it present clinically?

A

end = uremia

  • kidneys appear small, uniformly shrunken
  • hyalinzation of glomeruli
  • tubular atrophy
  • fibrous tissue in the dilated intersitium surrounds atrophic tubules
21
Q

How does diabetes mellitus affect the kidneys?

A

1 .Thickening of BM +

increased amount of mesangial matrix

= glomerulosclerosis

  1. basement membranes have increased permeability >> proteinuria
  2. arterioles have hyalinosis >> thickened walls and narrow lumens
  3. papillary necrosis
  4. prone to infections
22
Q

List the four most common forms of kidney stones.

A
  1. calcium
  2. struvite
  3. uric acid
  4. cystine
23
Q

Compare ascending and descending UTIs and list the most common predisposing conditions for these infections.

A
  • *Ascending**
  • bacteria introduced through urethra*
  • intrsumentation
  • intercourse
  • pregnancy
  • tumors
  • BPH

Descending
through blood

  • sepsis
  • septic emboli
24
Q

Compare the pathologic and clinical features of acute/chronic pyelonephritis.

A

Acute = suppurative infection of the kidneys

Chronic = may evolve from acute; persisten infection leads to the destruction of renal parenchyma and scar formation; loss of renal tissue; kidneys often asymmetric (b/c bacteria grow at different rates)

25
Q

Compare the causes of cystitis in men and women and in young and old people.

A

men

women

young

old

26
Q

Compare the pathologic and clnical features of acute and chronic cystitis.

A

acute = grossly visible congestion and mucosal hemorrhages (cystoscopy)

chronic = foci of hemorrhage, ulceration, thickening

27
Q

Explain how circulatory collapse causes renal tubular necrosis.

A

Sudden decrease in arterial pressure will result in acute hypoperfusion of the kidneys.

Key: **reduction of blood flow is more prominent in the CORTEX. Therefore, cortical tubules, especially PCT, are most affected. **

28
Q

Explain the effects of HTN on the kidneys

A
  • stimulates renal arterial and arteriolar contraction
  • thickening of vessel walls
  • arteries: fibrotic and multilayered
  • arterioles: hyalinazation

Malignant HTN >> fibrinoid necrosis (sustained will >> hyperplasia of smooth muscles, crescentic layer like onion ring)

arterial and arteriolar changes lead to ischemia >> renal failure

29
Q

List three common tumors of the urinary tract.

A
  1. renal cell carcinoma
  2. urothelial carcinoma
  3. Wilm’s tumor

*bladder tumors are the most common

30
Q

Compare renal cell carcinoma and Wilms’ tumor.

A

RCC = most common kidney cancer

  • possibly caused by smoking, link with VHL syndrome (loss of VHL tumor suppressor gene, characterized by appearance of cerebellar hemangioblastomas and retinal angiomas)*
  • sharply demarcted nodules and masses
  • cuboidal cells
  • “clear cell carcinoma”

**Wilm’s **= most common tumor in children

  • Two tumor suppressor genes **WT1 and 2, **appear to be transcription factor involved in the normal dev. of kidney/organs. Deletion = congenital malformations (often bilateral)*
  • immature cells
  • resemble fetal tubules and glomeruli
31
Q

Compare urothelial carcinoma of the renal pelvis and renal cell carcinoma.

A

Urothelial carcinoma = renal pelvis

resemble transitional carcinoma

RCC = most common kidney cancer

  • possibly caused by smoking, link with VHL syndrome (loss of VHL tumor suppressor gene, characterized by appearance of cerebellar hemangioblastomas and retinal angiomas)*
  • sharply demarcted nodules and masses
  • cuboidal cells
  • “clear cell carcinoma”
32
Q

How common is carcinoma of the urinary bladder?

A

= most common urinary tract cancer

3x more common in males

33
Q

Correlate the macroscopic and microscopic features of urinary bladder carcinoma with the clinical features of this tumor.

A

May be _papillary or flat_. Papillary = wartlike, flat = mucosal thickenings. Either may be i_nvasive or noninvasive. _

_Papillary _

​low or high grade:

  • low = lined by uniform cells
  • high = mitotic, pleomorphic, hyperchromatic

Flat

carcinoma in situ or invasive

  • anaplastic, resemblance to urethelial mucosa

Squamous/adeno

preceded by squamous/glandular metaplasia

sarcomas

from smooth muscular bladder wall

  1. flat high-grade malignancy, carcinoma in situ
  2. papillary tumor confined to urothelium (Ta)
  3. papillary tumor invading lamina propria (T1)
  4. papillary and invasive tumor involving muscle (T2)
  5. invasive tumor extending through perivesical fat (T3)
34
Q

What are the typical symptoms of urinary bladder carcinoma?

A

clinical: hematuria, dysuria, low abd pain

35
Q

What is the outcome of treatment of urinary bladder carcinoma?

A 
**Treatment: **surgical resection, chemo
also immunotherapy (intravesical, BCG)

low grade tumors tend to recur

Stage 1 low grade, no invasion = 95% 10 yr survival

Invasion of muscle layer = 25% mortality

36
Q

Clinical features of acute glomerulonephritis

A

Damaged basement membranes of the inflamed glomeruli become permeable >> proteinuria + hematuria

decreased GFR >> oliguria

loss of protein >> edema

reduced blood flow lead to inflamed glomeruli, release of renin >> HTN

37
Q

Goodpasture’s syndrome

A

Autoimmune disease characterized by formation of antibodies to the body’s own basement membrane component: _ collagen type IV_

Causes intralveolar hemorrhage + ruptured glomerular basement membranes

  • macrophages exit through the holes in the BM, accumultate in the urinary space >> crescents that compress the capillary loops = anuria*
  • = rapidly progressive glomeruonephritis*

Pathology (16 decks)

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