3rd Shifting Kidneys, Lower Urinary Tract and Male Urinary Tract Flashcards

1
Q

Four basic morphologic components of the kidneys

A

Glomeruli
Interstitium
Tubules
Blood vessels

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2
Q

biochemical abnormality that refers to elevation of the BUN and creatinine levels

A

Azotemia

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3
Q

Azotemia + clinical signs and symptoms

A

Uremia

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4
Q

Examples of uremic symptoms

A

anorexia, lethargy, dec mental acuity, coma

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5
Q

Nephritic syndrome is a glomerular disease dominated by the acute onset of what symptoms?

A

▪grossly visible hematuria
▪mild to moderate proteinuria
▪hypertension

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6
Q

Examples of diseases associated/presenting with Nephritic syndrome

A
  1. Post streptococcal glomerulonephritis
  2. Rapidly progressive (Crescentic) glomerulonephritis
  3. Goodpasture’s syndrome
  4. Glomerulonephritis with vasculitis
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7
Q

Characteristic symptoms in Nephrotic Syndrome

A

Heavy proteinuria (>3.5 g/day), hypoalbuminemia, severe edema, hyperlipidemia and lipiduria

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8
Q

Examples of diseases associated/presenting with Nephrotic syndrome

A
  1. Lipoid nephrosis
  2. Focal segmental glomerulosclerosis
  3. Membranous glomerulosclerosis
  4. Diabetic nephropathy
  5. Amyloidosis
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9
Q

Oliguria or anuria and recent onset of azotemia

A

Acute renal failure

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10
Q

Prolonged signs and symptoms of uremia

A

Chronic renal failure

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11
Q

End result of chronic renal parenchymal diseases

A

Chronic renal failure

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12
Q

Characteristic symptoms of Renal tubular defects

A

polyuria, nocturia and electrolytes disorders

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13
Q

examples of diseases presenting with renal tubular defects

A
  1. Inherited (familial nephrogenic diabetes, cystinuria, renal tubular acidosis)
  2. Acquired (lead nephropathy)
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14
Q

Characteristic symptoms of UTI

A

Bacteriuria, Pyuria

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15
Q

Characteristic symptoms of Nephrolithiasis

A

Severe spasm of pain (renal colic) and hematuria

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16
Q

What disease is characterized by Nephritic symptoms with a rapid decline in GFR (hours-days)

A

Rapid Progressive (Crescentic) Glomerulonephritis

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17
Q

major cause of death from renal diseases

A

Chronic Renal Failure

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18
Q

4 stages of renal disease

A
  1. Diminisehed renal reserve (50%GFR)
  2. Renal insufficiency (20%-50% GFR)
  3. CRF (20%-25% GFR)
  4. End stage renal Disease (<5% GFR)
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19
Q

What are the symptoms of Renal insufficiency (Stage II)

A

polyuria, hypertension, nocturia, anemia, azotemia

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20
Q

What are the symptoms of CRF (Stage III)

A

Uremia, edema, metabolic acidosis, hyperkalemia

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21
Q

most common causes of Chronic Kidney Disease

A

Chronic Glumerulonephritis

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22
Q

What are the clinical manifestations of Glomerular Disease

A

Nephritic, Nephrotic, RPGN, CRF, isolated urinary abnormalities

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23
Q

Histologic alterations in glomerular diseases (4)

A
  • Hypercellularity
  • Basement Membrane Thickening
  • Hyalinization/Hyalinosis
  • Sclerosis
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24
Q

Proliferating parietal cells and infiltrating leukocytes

A

Crescents (Present in hypercellularity)

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25
Q

Deposition of amorphous electron dense materials in the endothelial or epithelial side of the basement membrane

A

Basement Membrane Thickening

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26
Q

Hyalinization of glomerulus is a common feature in what disease?

A

Focal segmental glomerolusclerosis

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27
Q

Accumulation of extracellular collagenous matrix, either confined to the mesangial areas (DM) or involving the capillary loops

A

Sclerosis

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28
Q

Pathogenesis of Glomerular Injury (How are they injured?)

A

ANTIBODY-MEDIATED INJURY
CYTOTOXIC ANTIBODIES
CELL-MEDIATED IMMUNE INJURY
ACTIVATION OF ALTERNATIVE COMPLEMENT PATHWAY

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29
Q

Forms of Antibody Mediated Glomerular Injury:

A
  1. Intrinsic (Immune complex deposition involving intrinsic and in situ renal antigens)
  2. Extrinsic (Circulating Immune complex Glumerulonephritis)
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30
Q

Examples “Immune complex deposition involving intrinsic and in situ renal antigens” form of glomerular injury

A
  1. Heymann Nephritis (granular)
  2. Ab against planted Antigens (granular)
  3. Anti GBM Ab-induced GN (linear)
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31
Q

Granular immune deposits in the visceral epithelium

A

Heymann Nephritis

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32
Q

Ab to component of the GBM

Masugi or nephrotoxic nephritis

A

Anti GBM Ab-induced GN

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33
Q

what happens to:

a. Cationic immunogens
b. Anionic immunogens
c. Neutral immunogens

A

a. cross the BM and are deposited in the subepithelium
b. trapped subendothelially or NOT nephritogenic
c. deposited in the mesangium

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34
Q

Mediators of Glomerular Cellular Injury

A

Celllular mediators:
Neutrophils, T cells, Platelets, mesangial cells
Soluble mediators:
Complement, eicosanoids, cytokines, chemokines, coagulation system

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35
Q

Two major histologic characteristics of progressive renal damage:

A
  1. Focal Segmental Glomerulosclerosis (FSGS)

2. Tubulointersititial fibrosis

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36
Q

develop proteinuria even if the primary dse was non glomerular

A

Focal Segmental Glomerulosclerosis (FSGS)

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37
Q

adaptive change that occurs in the unaffected glomeruli of diseased kidneys; Compensatory hypertrophy of the remaining glomeruli

A

Glomerulosclerosis

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38
Q

in Tubulointerstitial Fibrosis, what is the cause of direct injury to and activation of tubular cells

A

Proteinuria

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39
Q

Primary Glomerulopathies (8)

A
 Nephritic syndrome
 Nephrotic syndrome
 Membranous nephropathy
 Minimal-change disease
 HIV-associated nephropathy
 RPGN
 FSGS
 MPGN
40
Q

2 types of Acute Proliferative GN

A
  1. Poststreptococcal GN

2. Post-infectious GN

41
Q

Syndrome associated with severe glomerular injury ;NOT a specific etiologic form of glomerulonephritis

A

RPGN (Crescentic GN)

42
Q

Rapid and progrssive loss of renal function associated with severe oliguria and signs of nephritic syndrome

A

RPGN (Crescentic GN)

43
Q

Enlarged kidneys with petechial hemorrhages on its cortical surface

A

RPGN (Crescentic GN)

44
Q

Type 1 RPGN characteristics:

A
  • Anti-GBM Antibody
  • Antigen: noncollagenous portion of the α3 chain of collagen type IV
  • Linear deposits of IgG
  • C3 in the GBM
45
Q

Type 2 RPGN characteristics:

A
  • Immune Complex deposition

- Granular pattern of staining

46
Q

Type 3 RPGN characteristics:

A
  • Pauci-Immune
  • ANCA-associated
  • Lack of anti-GBM antibodies or immune complexes
47
Q

amount of massive proteinuria in Nephrotic syndrome

A

3.5 g/day

48
Q

Most common cause of nephrotic syndrome among adults

A

Focal Segmental Glomerulosclerosis

49
Q

Diffuse thickening of the glomerular capillary wall due to accumulation of electron dense, Ig containing deposits along the subepithelial side of the basement membrane

A

Membranous Nephropathy

50
Q

Most frequent cause of nephrotic syndrome in children

A

Minimal change disease

51
Q

Diffuse loss of foot processes (podocytes) in most glomeruli (“Fusion” of foot processes)

A

Minimal change disease

52
Q

Cells of proximal tubules are often laden with lipid and protein which reflect tubular reabsorption of lipoproteins passing through diseased glomeruli

A

Lipoid Nephrosis

53
Q

 Morphologic variant of FSGS; Retraction and/or collapse of the entire glomerular tuft, with or without additional FSGS lesions

A

Collapsing Glomerulopathy

54
Q

Characteristic feature of Collapsing Glomerulopathy

A

proliferation and hypertrophy of glomerular visceral epithelial cells

55
Q

Secondary form of FSGS

A

RENAL ABLATION FSGS

56
Q

Striking focal cystic dilation of tubule segments

A

HIV-associated Nephropathy

57
Q

Presence of large numbers of tubuloreticular inclusions within endothelial cells

A

HIV-associated Nephropathy

58
Q

Proliferation is dominant in the mesangium but may involve the capillary loops

A

MPGN or Mesangiocapillary glomerulonephritis

59
Q

Type 1 MPGN characteristics:

A
  • Activation of both classical and alternative complement pathways
  • Granular pattern
  • Antigens are believed to be proteins derived from infectious agents such as hepatitis C and B viruses
60
Q

Type 2 MPGN characteristics:

A
  • activation of the alternative complement pathway
  • Lamina densa of GBM – ribbon-like
  • Mesangial rings – characteristic circular aggregates In the mesangium
61
Q

ISOLATED URINARY ABNORMALITIES

A
 IgA nephropathy (Berger’s disease)
 Hereditary nephritis
 Alport syndrome
 Thin basement membrane lesion (Benign Familial Hematuria)
 Chronic glomerulonephritis
62
Q
  • Presence of prominent IgA deposits in the mesangial regions
  • most common type of glomerulonephritis worldwide
A

IgA nephropathy (Berger’s disease)

63
Q

Refers to a group of heterogeneous familial renal diseases associated primarily with glomerular injury

A

Hereditary nephritis

64
Q

Hereditary nephritis (2)

A
  1. Alport Syndrome

2. Thin basement membrane lesion

65
Q

Symptoms of Alport syndrome

A
  • Nerve Deafness
  • Lens Dislocation
  • Posterior cataracts
  • Corneal Dystrophy
66
Q
  • Due to abnormal α3 (COL4A3), α4 (COL4A4), or α5 (COL4A5) chain of type IV collagen
  • X-linked
  • Basket-weave appearance of the GBM
A

Alport Syndrome

67
Q
  • familial asymptomatic hematuria

- Mutations in genes encoding α3 or α4 chains of type IV collagen

A

Thin basement membrane lesion

68
Q
  • Considered a pool of end-stage glomerular disease

- Obliteration of glomeruli, transforming them into acellular eosinophilic masses

A

Chronic GN

69
Q

GLOMERULAR LESIONS ASSOCIATED WITH SYSTEMIC DISEASES

A
 Lupus Nephritis
 Henoch-Schönlein Purpura
 Bacterial Endocarditis–Associated Glomerulonephritis
 Diabetic Nephropathy
 Amyloidosis
 Fibrillary Glomerulonephritis
70
Q

Affects the arterioles – causing Hyalinizing Arteriolar Sclerosis

A

Diabetic Nephropathy

71
Q

Three glomerular syndromes of Diabetic Nephropathy

A

o Non-nephrotic proteinuria
o Nephrotic syndrome
o Chronic renal failure

72
Q

Fibrillary deposits in the mesangium and capillary tufts that resembles amyloid but does not stain with congo-red

A

Fibrillary Glomerulonephritis

73
Q

Congo red-fibrillary amyloid deposits – present in the mesangium and capillary walls

A

Amyloidosis

74
Q

Two major groups of TUBULAR AND INTERSTITIAL DISEASES

A
  1. Acute Kidney Injury and Acute Renal Failure

2. Tubulointerstitial Nephritis

75
Q

Most common cause of acute renal failure

A

Acute Kidney Injury and Acute Renal Failure

76
Q

Symptoms of the Maintenance phase of AKI/ATI

A

a. Sustained decreases in urine output to 40-400 mL/day (oliguria)
b. salt and water overload
c. rising BUN
d. Hyperkalemia
e. Metabolic Acidosis
f. Other manifestations of Uremia

77
Q

relatively short lengths of tubules are affected, and straight segments of proximal tubules (PST) and ascending limbs of Henle’s loop (HL) are most vulnerable

A

Ischemic AKI/ATI

78
Q

extensive necrosis is present along the proximal convoluted tubule segments (PCT) with many toxins (e.g., mercury), but necrosis of the distal tubule, particularly ascending HL, also occurs

A

Toxic AKI/ATI

79
Q

Diffuse interstitial, predominantly, mononuclear inflammatory infiltrate; Tubules are separated by inflammation and edema

A

Tubulointerstitial Nephritis

80
Q

Renal disorder affecting the tubules, interstitium, and renal pelvis

A

Pyelonephritis

81
Q

most common cause of clinical pyelonephritis

A

Ascending infection

82
Q

Complications of Acute Pyelonephritis

A

o Papillary necrosis
o Pyonephrosis
o Perinephric abscess

83
Q

2 forms of Chronic Pyelonephritis

A

o Reflux nephropathy

o Chronic obstructive pyelonephritis

84
Q

Unusual and relatively rare form of chronic pyelonephritis; Accumulation of foamy macrophages intermingled with plasma cells, lymphocytes, polymorphonuclear leukocytes, and occasional giant cells
yellow-orange nodules

A

XANTHOGRANULOMATOUS PYELONEPHRITIS

85
Q

Vascular diseases of the Kidneys

A
 Benign Nephrosclerosis
 Malignant hypertension (Accelerated Nephrosclerosis)
 Renal Artery Stenosis
 Thrombotic microangiopathies
 Atherosclerotic Ischemic Renal Disease
 Atheroembolic Renal Disease
 Sickle Cell Disease Nephropathy
 Diffuse cortical necrosis
 Renal Infarcts
86
Q
  • Sclerosis of the renal arterioles and small arteries

- Reduction in functional renal mass caused by glomerulosclerosis and chronic tubulointerstitial injury

A

Benign Nephrosclerosis

87
Q

Long-standing benign hypertension with eventual injury to the arteriolar walls or the initiating injury may spring de novo from arteritis, a coagulopathy, or some injury causing acute exacerbation of the hypertension

A

Malignant hypertension (Accelerated Nephrosclerosis)

88
Q
  • Gross: “flea-bitten” appearance

- Onion-skinning because of its concentric appearance (hyperplastic)

A

Malignant hypertension (Accelerated Nephrosclerosis)

89
Q

Most common cause of renal artery stenosis (70% of cases) is _____________ at the origin of the renal artery

A

occlusion by atheromatous plaque

90
Q

Congenital Anomalies of the Kidneys

A

o Agenesis of the kidney
o Hypoplasia
o Ectopic Kidneys
o Horseshoe Kidneys

91
Q

Due to an abnormality in metanephric differentiation
-Persistence in the kidney of abnormal structures—cartilage, undifferentiated mesenchyme, and immature collecting ductules

A

MULTICYSTIC RENAL DYSPLASIA

92
Q

term used to describe dilation of the renal pelvis and calyces associated with progressive atrophy of the kidney due to obstruction of the outflow of urine

A

Hydronephrosis

93
Q

increased urinary concentration of the stones’ constituents, such that it exceeds their solubility (supersaturation)

A

UROLITHIASIS (RENAL CALCULI/STONES)

94
Q

Staghorn calculi

A

MAGNESIUM AMMONIUM PHOSPHATE

95
Q

Benign Tumors of the kidneys

A

Renal papillary adenoma
Renal fibroma or hamartoma (Renomedullary interstitial cell tumor)
Angiomyolipoma
Oncocytoma

96
Q

Malignant Tumors of the kidneys

A

Renal cell carcinoma

Urothelial carcinoma of the renal pelvis

97
Q

Most common Malignant Tumor of the kidneys

A

Renal cell carcinoma