(2.1) Renal Pathology 1: Renal and Male GU (Putthoff) Flashcards

1
Q

General functions of the kidneys?

A
  • Excrete certain waste products of metabolsim
  • Regulates the body’s concentration of water, salt, calcium and phosphorous
  • Maintains acid balance of plasma
  • Serves as an endocrine organ
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2
Q

_________ is the most common cause of CRF/ESRD

__________ is the second most common cause

A

Diabetes is the most common cause of CRF/ESRD

High blood pressure is the second most common cause

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3
Q

Which kidney is higher? Left or right?

A

Left is higher!!!

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4
Q

What is a good spinal marker for the location of the kidneys?

A

T12

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5
Q

Why is the right kidney lower than the left?

A

Liver pushes down on the right kidney

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6
Q

How do most diseases/disorders of the kidney present?

A

Hematuria

Proteinuria

Edema

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7
Q

What is the single most important question to ask a patient suspected of having renal disease?

A

“Have you had this before?”

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8
Q

What are some of the common imaging techniques of the kidney and associated GU organs?

A

Ultrasonography

KUB - plain abdominal film

CT Scan

MRI, MRA

Radionuclide imaging

Renal angiography

Renal tomography

IVP

Retrograde pyelography

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9
Q

What techniques are used to evaluate the ureter, bladder or urethra?

A

Cystography

Voiding cytourethrography

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10
Q

What are some techniques utilized on renal biopsy material?

A

Light microscopy

Fluorescence microscopy

Electron microscopy

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11
Q

State the commonly associated pathology with the anatomical structure:

Glomeruli =

Tubules =

Interstitium =

Vessels =

A

Glomeruli = Glomerulonephritis

Tubules = Bence-Jones protinuria

Interstitium = Fibrosis, inflammation or edema

Vessels = Vasculitis, nephrosclerosis

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12
Q

Define:

Azotemia

A
  • Biochemical abnormality indicating an elevation of blood urea nitrogen (BUN) and creatinine levels
  • Usually related to a decreased GFR
  • Generally the result of renal disorders
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13
Q

How can azotemia arise?

A

Arises from one of two categories:

1) Prerenal azotemia
2) Postrenal azotemia

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14
Q

What is prerenal azotemia?

A

Occurs after hypoperfusion of kidneys

Arises after shock, volume depletion and CHF that impairs renal function in the absence of primary renal parenchymal damage

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15
Q

What is postrenal azotemia?

A

Seen whenever urine flow is obstructed DISTAL to the calyces and renal pelvis

*Removal of obstruction corrects the azotemia

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16
Q

What is uremia?

A

Azotemia PLUS a constellation of clinical findings and biochemical abnormalities resulting from renal damage

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17
Q

What are the signs/symptoms of uremia?

A
  • N/V, weight loss, fatigue, anorexia
  • Pruritus
  • Polydipsia
  • Electrolyte abnormalities
  • Encephalopathy
  • Bleeding manifestations due to platelet dysfuction
  • Pericarditis
  • Pleuritis/pleural effusion
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18
Q

What’s a normal GFR rate?

A

90-120 mL/min

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19
Q

What is acute kidney injury (AKI)?

A
  • Rapid decline in GFR
  • SEVERE forms exhibit oliguria or anuria
  • May result from glomerular, interstitial, vascular or acute tubular injury (ATN)
  • Can be reversible
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20
Q

What is chronic kidney disease (CKD)?

A
  • Mild (clinically silent)
  • Defined with diminished GFR
  • Persistent albuminuria
  • CKD is generally irreversible
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21
Q

Define:

End stage renal disease (ESRD)

A

GFR <5% of normal

End stage of uremia

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22
Q

Define:

Nephrotic syndrome

A

Glomerular disease characterized by severe proteinuria (more than 3.5 gm/day – (less in children)), hypoalbuminemia, severe edema, hyperlipidemia, and lipiduria

23
Q

Define:

Nephritic syndrome

A

Glomerular disease dominated by acute onset of grossly visible hematuria, mild to moderate proteinuria, and hypertension

24
Q

Define:

Rapidly progressive glomerulonephritis (RPGM)

A

Signs of nephritic syndrome with rapid delcine (days-weeks) in GFR

Implies severe glomerular injury

25
Q

Define:

Isolated urinary abnormalities

A

Glomerular hematuria and/or subnephrotic range proteinuria

26
Q

Associate the syndrome with the manifestations:

Hematuria, azotemia, oliguria, edema, hypertension

A

Nephritic syndrome

27
Q

Associate the syndrome with the manifestations:

>3.5 gm/day proteinuria, hypoalbuminemia, hyperlipidemia, lipiduria

A

Nephrotic syndrome

28
Q

Associate the syndrome with the manifestations:

Acute nephritic, proteinuria, and acute renal failure

A

Rapidly progressive glomerulonephritis

29
Q

Associate the syndrome with the manifestations:

Azotemia –> uremia progressing for months to years

A

Chronic renal failure

30
Q

Associate the syndrome with the manifestations:

Glomerular hematuria and/or subnephrotic proteinuria

A

Isolated urinary abnormalities

31
Q

What are the pathologic responses of the glomerulus to injury?

A

Hypercellularity (inflammatory, crescents)

Basement membrane (thickening, deposits)

Hyalinosis and Sclerosis

32
Q

Descriptive patterns/distributions in the categorization of glomerular disorders:

Diffuse?

A

Diffuse involves all glomeruli

33
Q

Descriptive patterns/distributions in the categorization of glomerular disorders:

Focal?

A

Focal involves only a subset of glomeruli

34
Q

Descriptive patterns/distributions in the categorization of glomerular disorders:

Segmental?

A

Segmental of affected glomeruli, only portions are involved

35
Q

Descriptive patterns/distributions in the categorization of glomerular disorders:

Global?

A

Global involves entire glomerulus

36
Q

Table 20-5

A

Memorize? I guess. Sure.

37
Q

LOOK UP THESE CONCEPT BOXES

A

Nephritic syndrome (key concepts page 913)

Nephrotic syndrome (key concepts page 922)

Isolated glomerular abnormalities (key concepts page 925)

38
Q

What is the population commonly associated with acute proliferative glomerulonephritis?

A

Children

39
Q

Describe acute proliferatie glomerulonephritis

Signs?

A

Immune complex injury trigged by exogenous bacterial, viral or fungal antigen

  • Marked hypercellularity
  • Leukocyte infiltration
40
Q

What do we commonly see in acute proliferative glomerulonephritis on electron microscopy?

A

Subepithelial “hump” of immune complex

41
Q

What frequently causes acute proliferative glomerulonephritis?

A

Strep B

42
Q

Describe the histologic differences b/w a normal glomerulus and a RPGN glomerulus

A

Collapsed, compacted glomerular tufts

Crescent-shaped mass of proliferating visceral and parietal epithelial cells

43
Q

Anti-Glomerular Basement Membrane Disese

“Goodpasture syndrome”

What is it?

A

Type 1 RPGN is an anti-GBM antibody induced disease, characterized by linear deposits of IgG and in many cases, C3 in the GBM

44
Q

Anti-Glomerular Basement Membrane Disese

“Goodpasture syndrome”

Clinically, what occurs?

A

Pulmonary hemorrhage occurs in addition to renal disease

45
Q

Define:

Nephrotic syndrome

A

A renal syndrome in which the basic defect is increased permeability of glomeruli to plasma proteins

Resulting in PROTEINURIA

46
Q

What are the major clinical findings associated with nephrotic syndrome?

A

Severe proteinuria >3.5gm/24hrs

Hypoalbuminemia <3.0gm/dL

Edema

Hyperlipidemia

47
Q

Most common cause of nephrotic syndrome in primary glomerular disease in CHILDREN?

A

Minimal-change disease

48
Q

What is the main difference b/w primary and secondary renal disease?

A

Primary: comes from renal etiology

Seconday: comes from systemic diseases (DM, SLE)

49
Q

Describe the histologic changes you’d see with membranous glomerulopathy

A

Marked diffuse thickening of capillary walls without increase in cellularity

50
Q

What are the characteristics of minimal change disease (MCD)?

A

Edema

Peak incidence b/w 2-6 y/o

MCD is the most common cause of NS in children and may follow a respiratory infection or immunization

51
Q

What is considered a therapy and diagnostic intervention for minimal change disease (MCD)?

A

Dramatic response to corticosteroid therapy

52
Q

Yet another table to “memorize”

A

Yay.

53
Q

Membranoproliferative GN (MPGN) is best considered a _______________ injury rather than a specific disease

A

Membranoproliferative GN (MPGN) is best considered a pattern of immune-mediated injury injury rather than a specific disease

54
Q

*Protip:

Use Erik’s flashcards for the details of the lecture. He made them based off of the robbins chapter

A