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CRP- Renal > Pathology of Glomerular Disease I > Flashcards

Pathology of Glomerular Disease I Flashcards

1
Q

What is acute renal failure?

A

acute, severe decrease in renal function (develops within days). Hallmark is AZOTEMIA= increased nitrgoenous waste products in the blood; BUN and creatinine (Cr), often with oliguria (low production of urine).

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2
Q

What are the 3 etiologies (causes) of acute renal failure?

A
  1. prerenal azotemia= decreased blood flow to kidneys (common cause of ARF).
  2. postrenal azotemia= obstruction of utrinary tract downstream (i.e. ureters).
  3. intrarenal azotemia
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3
Q

What happens to GFR in any case of acute renal failure?

A

it DECREASES

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4
Q

What will the serum BUN: Cr ratio rise to in prerenal azotemia?

A

> 15, because RAAS will be triggered due to low blood flow, thus causing aldosterone to increase Na+ and water reabsorption. BUN will be reabsorbed with the water, but Cr cannot. So BUN will rise in the blood.

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5
Q

Will the tubular function remain intact with prerenal azotemia?

A

YES, because we haven’t damaged the tubular cells in this case. So the fractional excretion of Na+ (FENa) will be less than 1%. This indicates that the tubules are able to absorb Na+. Also urine osmolality will be >500 mOsm/kg indicating that the tubules are able to concentrate the urine.

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6
Q

What happens in the EARLY stage of postrenal azotemia?

A

increased tubular pressure forces BUN into the blood serum (serum BUN:Cr > 15).

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7
Q

Will the tubular function remain intact in the EARLY stage of postrenal azotemia?

A

YES just like prerenal azotemia (FENa 500 mOsm/kg).

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8
Q

What happens with long-standing obstruction of postrenal azotemia?

A

tubular damage ensures, resulting in decreased reabsorption of BUN (serum BUN:Cr 2%), and inability to concentrate urine (urine osm

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9
Q

What are the 3 causes of intrarenal azotemia?

A
  1. acute tubular necrosis
  2. acute interstitial nephritis
  3. renal papillary necrosis
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10
Q

What is acute tubular necrosis (a cause of intrarenal azotemia)?

A

injury and necrosis of tubular epithelial cells. This is the most common cause of acute renal failure (ARF). Necrotic cells plug tubules, and this obstruction decreases GFR.

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11
Q

What is a classic hallmark of acute tubular necrosis?

A

brown, granular casts in the urine from sloughing off the the dead and necrotic tubular cells into the urine.

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12
Q

Will the BUN:Cr ratio be greater than or less than 15 in acute tubular necrosis?

A
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13
Q

What will happen to the FENa and urine concentration in acute tubular necrosis?

A

FENa > 2% and urine osm

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14
Q

What are the 2 etiologies (causes) of acute tubular necrosis?

A
  1. ischemic

2. nephrotoxic

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15
Q

What happens in ischemic acute tubular necrosis?

A
  • decreased blood supply results in necrosis of tubules. It is often preceded by prerenal azotemia.
  • The PCT and medullary segment of the thick ascending limb are most susceptible (bc they require a lot of ATP).
  • will see increased vasoconstriction.
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16
Q

What happens in nephrotoxic acute tubular necrosis?

A

toxic agents result in necrosis of tubules. The PCT is most susceptible.

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17
Q

What are the causes of nephrotoxic acute tubular necrosis?

A
  • aminoglycosides (most common)
  • heavy metals (lead)
  • myoglobinuria (crush injury to muscle)
  • ethylene glycol; antifreeze (associated with oxalate crystals in the urine).
  • radiocontrast dye
  • urate (tumor lysis syndrome from chemotherapy. To avoid this keep pts hydrated and administer allopurinol).
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18
Q

What are the clinical features of acute tubular necrosis?

A
  • oliguria with brown, granular casts (Tamm-Horsfall proteins with the ischemic type).
  • elevated BUN and Cr (due to low GFR preventing filtering of BUN and creatinine).
  • hyperkalemia (due to decreased renal excretion) with metabolic acidosis.
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19
Q

Is acute tubular necrosis reversible?

A

YES, but often requires supportive dialysis since electrolyte imbalances can be fatal.

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20
Q

How long can oliguria persist following acute tubular necrosis?

A

2-3 weeks because the PCT cells are stable cells that take time to reenter the cell cycle and regenerate.

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21
Q

What is acute interstitial nephritis (a cause of intrarenal azotemia)?

A

drug-induced hypersensitivity involving the interstitium and tubules. The drugs include NSAIDs, penicillin, and diuretics.

22
Q

How does acute interstitial nephritis present?

A

oliguria, fever, and rash days to weeks after starting a drug. EOSINOPHILS will be present and may be seen in the urine. This will resolve with cessation of the drug, but may progress to renal papillary necrosis.

23
Q

What is renal papillary necrosis (a cause of intrarenal azotemia)?

A

necrosis of renal papillae presenting with gross hematuria and flank pain.

24
Q

What are the causes of renal papillary necrosis?

A
  • chronic analgesic abuse (long-term phenacetin or aspirin use).
  • DM
  • sickle cell trait or disease
  • severe acute pyelonephritis
25
Q

What is the hallmark of NEPHRITIC syndrome?

A

glomerular inflammation and bleeding

26
Q

What will you see with NEPHRITIC syndrome?

A
  • limited proteinuria
  • HTN
  • oliguria and azotemia
  • RBC casts
27
Q

** What would a biopsy reveal in nephritic syndrome?

A

hypercellular, inflamed glomeruli, due to immune-complex deposition, which activates COMPLEMENT (C5a), attracting neutrophils (hence hypercellular), which mediate damage. You may also see basement membrane thickening of the glomerulus.

28
Q

What is the prototypic syndrome that results in nephritic syndrome?

A

poststreptococcal glomerulonephritis (PSGN). This arises after group A beta-hemolytic strep infection of the skin (impetigo) or pharynx.

29
Q

With what specific strains does PSGN occur?

A

nephritogenic strains= particular group A beta-hemolytic strain that carries M protein virulence factor.

30
Q

Can you develop nephritic syndrome after infection with nonstreptococcal organisms as well?

A

YES

31
Q

When does PSGN typically present?

picmonic

A

2-3 weeks after infection, as hematuria (cola-colored urine), oliguria, hypertension, and periorbital edema.
* Usually seen in children, but can be seen in adults.

32
Q

** What will you see on biopsy with PSGN?

A
  • hypercellular inflamed glomeruli from immune complex deposition seen on granular immunofluorescence, and SUBEPITHELIAL HUMPS on EM.
33
Q

What is the treatment for PSGN?

A

supportive and most cases will resolve in children.

In adults however, there is a risk to develop rapidly progressive glomerulonephritis (RPGN).

34
Q

What is rapidly progressive glomerulonephritis (RPGN)?

picmonic

A

nephritic syndrome that progresses to renal failure in weeks to months :(

35
Q

** What will a biopsy reveal in RPGN?

A

CRESCENTS in Bowman space on H&E stain; crescents are comprised of FIBRIN and MACROPHAGES (aka: inflammatory debris).

36
Q

What is the next thing you do after biopsy with someone who has RPGN?

A

immunofluorescence because this will help to resolve the etiology.

37
Q

** What are the 3 possible patterns you’ll see with immunofluorescence (IF) of RPGN?

A
  1. linear IF= antibody against the glomerular basement membrane, creating a sharp line on the fluorescence.
  2. granular IF
  3. negative IF (pauci-immune)
38
Q

** What key disease will be responsible for linear IF?

A

Goodpasture syndrome= antibody against collagen in glomerular and alveolar basement membranes. It presents as hematuria and hemoptysis (classically in young adult males).

39
Q

** What 2 key diseases will be responsible for granular IF?

high yield

A
  1. PSGN
  2. diffuse proliferative glomerulonephritis (Heymann nephritis)= diffuse antigen-antibody complex deposition, usually SUB-ENDOTHELIAL. This is the most common type of renal disease seen with SLE!!!!
40
Q

What test do you do if you get a negative IF for RPGN?

A

ANCA (anti-neutrophil cell antibody) test.
c-ANCA= Wegener granulomatosis (lung and kidney).
p-ANCA= microscopic polyangitits or Churg-Stauss syndrome

41
Q

What 3 things will you see in Churg-Strauss that you won’t see in microscopic polyangitis, in order to distinguish the two?

A
  1. granulomatous inflammation
  2. eosinophilia
  3. asthma
42
Q

What is IgA nephropathy (Berger’s disease)?

picmonic

A

IgA immune complex deposition in mesangium of glomeruli. This is the most common nephropathy WORLDWIDE!

43
Q

How does IgA nephropathy present?

A

during childhood as episodic gross or microscopic hematuria with RBC casts, usually following mucosal infections; duh bc IgA fights off mucosal infections (i.e. gastroenteritis). This may slowly progress to renal failure.

44
Q

What is Alport syndrome?

picmonic

A

inherited defect in type IV collagen (COL4A mutations); most commonly X-linked. It results in thinning and splitting of the glomerular basement membrane.

45
Q

How does Alport syndrome present?

A

isolated hematuria, sensory hearing loss, and ocular disturbances.

46
Q

What will you often see on histology in the end stages of glomerular disease?

A

hyalinization and sclerosis

47
Q

What terminology is good to know?

A
  • diffuse= involving all glomeruli
  • global= involving the entire glomerulus
  • focal= involving only some glomeruli
  • segmental= affecting a part of each glomerulus
  • mesangial= affecting predominantly the mesangial cells.
48
Q

For circulating immune complex nephritis (antigen-antibody already bound before entering the glomerulus), where do anionic vs cationic immunogens tend to deposit?

A
  • cationic= subepithelial
  • anionic= subendothelial
  • neutral= mesangium
49
Q

What is usually a good indication of basement membrane injury or damage to the podyctes in the glomerulus?

A

proteinuria

50
Q

** What is Henoch-Schonlein purpura?

picmonic

A
  • systemic vasculitis characterized by deposition of IgA immune complexes in skin, joints, GI, kidney, and other organs.
  • will see palpable purpura in the lower extremities.
  • gross microscopic hematuria and proteinuria
  • this often follows upper respiratory infection.
51
Q

** With what is systemic lupus erythematous (SLE) most of often associated?

A
  • NEPHRITIC syndrome. It affects young women (more African Americans), and is a multisystem disorder causing skin rashes, arthralgias, arthritis, inflamed serosal surfaces, renal, and CNS involvement.
52
Q

** Where do lupus immune complexes deposit in the glomerulus?

A
  • SUB-ENDOTHELIAL from DIFFUSE PROLIFERATIVE GLOMERULONEPHRITIS.
  • Classes I-IV (more areas become involved as you progress from I to IV).

CRP- Renal (19 decks)

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