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Perio Exam 2 > Renal 1 and 2 > Flashcards

Renal 1 and 2 Flashcards

1
Q

A. Glomeruli –

A

Network of capillaries between afferent arteriole (bringing blood to the capillary bed) and efferent arteriole (drains blood away from capillary bed).

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2
Q

Glomeruli: The capillary wall consists of

A

endothelium, basement membrane and epithelium (lining the urinary space).

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3
Q

Glomeruli: The epithelial cells have many finger-like processes that come from the cell body and contact the

A

basement membrane.

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4
Q

Glomeruli: A membrane connects adjacent processes (called the slit diaphragm) and is important in preventing

A

proteinuria.

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5
Q

Glomeruli: The capillary wall is permeable to

A

water and small molecules and impermeable to albumin and larger proteins.

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6
Q

Glomeruli capillaries are supported by connective tissue called the

A

mesangium.

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7
Q

Kidney Tubules – The filtrate from the glomeruli travels through the system of

A

tubules. The tubular epithelium reabsorbs some substances and secretes other substances, eventually forming urine

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8
Q

Kidney Interstitium – Formed by

A

collagen and blood vessels between the tubules and glomeruli.

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9
Q

Kidney Vasculature – The efferent arterioles supply the

A

capillary bed around some of the tubules (vasa recta). Absence of blood flow through the glomeruli reduces oxygen delivery to the tubules.

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10
Q
  1. Azotemia

Elevation of the

A

blood urea nitrogen (BUN) and creatinine levels, due to decreased filtration of blood through the glomeruli (decreased glomerular filtration rate).

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11
Q
  1. Uremia

Association of azotemia with

A

clinical signs and symptoms, including gastroenteritis, peripheral neuropathy, pericarditis, dermatitis, hyperkalemia, and metabolic acidosis.

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12
Q
  1. Acute nephritic syndrome: Results from
A

glomerular injury and is
characterized by acute onset of hematuria, mild to moderate
proteinuria, azotemia, and hypertension.

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13
Q
  1. Nephrotic syndrome:
A

Glomerular syndrome characterized by heavy

proteinuria (> 3.5 grams per day), hypoalbuminemia, severe edema, hyperlipidemia, and lipiduria.

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14
Q
  1. Acute renal failure:
A

Acute onset of azotemia with oliguria (or anuria).

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15
Q

Autosomal dominant (adult) polycystic kidney disease: 1. Clinical presentation:

A

seen in 1 out of every 500-1000 people,
characterized by multiple expanding cysts in both kidneys. Gradual onset of renal failure in adult, urinary tract hemorrhage (hematuria), pain, hypertension, urinary tract infection.

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16
Q

Autosomal dominant (adult) polycystic kidney disease: 2. Etiology: defective gene is

A

PKD1 (in 90% of families) located on

chromosome 16. The gene encodes for polycystin-1

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17
Q

Autosomal dominant (adult) polycystic kidney disease: 3. Extrarenal pathology:

A

1/3 of patients have cysts in liver; aneurysms

may develop in the circle of Willis (intracranial)

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18
Q

Autosomal dominant (adult) polycystic kidney disease: 4. Pathology:

A 
very large (up to 4 kg) kidneys with numerous cysts that
		arise in every part of the tubular system
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19
Q

Autosomal dominant (adult) polycystic kidney disease: 5. Histopathology

A

Cysts arise from all levels of the nephron

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20
Q

Autosomal dominant (adult) polycystic kidney disease: 6. Clinical:

A

flank pain around 4th decade, hematuria, hypertension and UTI, renal failure

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21
Q

B. Autosomal recessive (childhood) polycystic kidney disease: 1. Clinical:

A

renal failure develops from infancy to several years of age –
rare; seen in 1 in 20,000 live births. Due to mutations in the PKHD1
gene

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22
Q

B. Autosomal recessive (childhood) polycystic kidney disease: 2. Extrarenal pathology: almost all have

A

liver cysts and progressive liver fibrosis

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23
Q

B. Autosomal recessive (childhood) polycystic kidney disease: 3. Pathology:

A

numerous small uniform-size cysts from collecting tubules

in cortex and medulla

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24
Q

Mechanisms of glomerular injury

1. Immune complex deposits in

A

glomerular basement membrane (GBM)
or mesangium. These may result from circulating immune complexes that deposit in the glomerulus or circulating antibodies directed against glomerular components or non-glomerular antigens “planted” in the glomerulus.

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25
Q

Mechs of glomerular injury: 2. Epithelial and endothelial

A

cell injury.

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26
Q

B. Pathologic evaluation of kidney biopsies

1. Light microscopy -

A

In addition to H+E stain, PAS, trichrome and Jones stains are routinely done.

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27
Q

B. Pathologic evaluation of kidney biopsies: 2. Immunofluorescence -

A

Antibodies to immunoglobulin and complement, tagged with a fluorescent molecule, are used to identify immune complexes.

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28
Q

B. Pathologic evaluation of kidney biopsies: 3. Electron microscopy -

A

Identification of immune complexes, epithelial cell changes, basement membrane morphology and other changes.

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29
Q

Nephrotic syndrome

symptoms:

A

• Heavy proteinuria, hypoalbuminemia, severe edema (most obvious clinical sign), hyperlipidemia and lipiduria

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30
Q

Nephrotic syndrome caused by

A

• Caused by increased glomerular capillary permeability to plasma proteins:

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31
Q

Nephrotic syndrome: 1. Minimal change disease a) most common cause of

A

nephrotic syndrome in children.

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32
Q

Minimal change disease: b) pathology -

A

normal-appearing glomeruli by light microscopy; no immune complexes; electron microscopy demonstrates effacement of epithelial cell foot processes

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33
Q

Minimal Change disease: c) good response to

A

treatment (especially in children)

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34
Q
  1. Focal and segmental glomerulosclerosis: a) one of the most common causes of
A

nephrotic syndrome in adults.

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35
Q
  1. Focal and segmental glomerulosclerosis: b) Causes
A

primary (idiopathic) or secondary to other glomerular diseases, loss or scarring of other glomeruli, or genetic.

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36
Q
  1. Focal and segmental glomerulosclerosis: c) pathology
A
  • partial (segmental) sclerosis of some (focal) glomeruli characterized by increased mesangial matrix collagen with obliteration of capillary loops. The idiopathic form has no immune complexes.
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37
Q
  1. Focal and segmental glomerulosclerosis: d) poor response to
A

corticosteroid treatment – renal failure in 50% after 10 yrs.

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38
Q 
Membranous nephropathy (glomerulonephritis)
	     	a) most common in adults age
A

30-50

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39
Q

Membranous nephropathy (glomerulonephritis): b) Causes

A

primary (disease limited to the kidney) or secondary to infection, malignancy, SLE, or drugs.

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40
Q

Membranous nephropathy (glomerulonephritis): c) pathology -

A

immune complexes in the epithelial side (subepithelial) of the GBM demonstrable by immunofluorescence and electron microscopy

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41
Q

Membranous nephropathy (glomerulonephritis): d) poor response to

A

corticosteroid treatment, with 40% developing

renal failure in 2-20 years

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42
Q
  1. Glomerular disease in diabetes mellitus (see pp. 746-7): a) minimal proteinuria progresses, over
A

10-15 years, to severe proteinuria.

•

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43
Q
  1. Glomerular disease in diabetes mellitus (see pp. 746-7): b) thick glomerular basement membranes, diffuse increase in
A

mesangial matrix and formation of mesangial nodules (the latter is nodular glomerulosclerosis or Kimmelstiel-Wilson lesion). Other changes Hyaline arteriolosclerosis, Atherosclerosis, Nephrosclerosis

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44
Q

D. Nephritic Syndrome: • Characterized by acute onset of

A

1) hematuria, 2) oliguria & azotemia and 3) hypertension

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45
Q

Nephritic syndrome: • Proliferation of cells within the

A

glomeruli, accompanied by inflammatory cells

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46
Q

Nephritic syndrome: • Inflammation severely injures

A

capillary walls

• Results in blood passing into the urine as well as reduced GFR

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47
Q

. Acute postinfectious (poststreptococcal) glomerulonephritis
a) most commonly occurs in

A

children 1-4 weeks after a bout of streptococcal pharyngitis (other infections as well)

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48
Q

. Acute postinfectious (poststreptococcal) glomerulonephritis: b) pathology -

A

proliferation of endothelial and mesangial cells; infiltration of neutrophils and monocytes; immune complexes in GBM and sometimes in the mesangium.

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49
Q

. Acute postinfectious (poststreptococcal) glomerulonephritis: c) progression to chronic renal disease is more likely in

A

adults.

50
Q

IgA nephropathy

a) usually occurs in

A

children and young adults

51
Q

IgA nephropathy: b) hematuria is noted

A

1-2 days after non-specific upper respiratory

tract viral infection.

52
Q

IgA nephropathy: : c) pathogenesis may involve

A

increased IgA production

53
Q

IgA nephropathy: d) when the glomerular disease is associated with systemic manifestations (purpuric skin rash and arthritis), this is called

A

Henoch-Schönlein purpura.

54
Q

IgA nephropathy: e) pathology - mesangial deposition of immune complexes containing

A

IgA and variable proliferation of mesangial and endothelial cells. Occasionally there is epithelial cell proliferation with crescents.

55
Q

E. Crescentic or Rapidly Progressive Glomerulonephritis: • Acute clinical syndrome, not a specific form of

A

glomerulonephritis

56
Q

E. Crescentic or Rapidly Progressive Glomerulonephritis: • Progressive loss of

A

renal function; lab finding c/w nephritic syndrome; severe oligouria

57
Q

E. Crescentic or Rapidly Progressive Glomerulonephritis: • Death from renal failure in

A

weeks to months if untreated

58
Q

E. Crescentic or Rapidly Progressive Glomerulonephritis: • Characteristic finding is

A

crescentic glomerulonephritis due to proliferation of epithelial cells with infiltration of histiocytes

59
Q

E. Crescentic or Rapidly Progressive Glomerulonephritis: • Several different disorders:

A
  • Anti-GBM antibody disease (12% of cases)
  • Immune complex disease (44% of cases)
  • Pauci-immune, lack of anti-GBM or immune complexes (44% of cases)
60
Q

Crescentic or Rapidly Progressive Glomerulonephritis

  1. May be associated with
A

antibodies directed against a glomerular basement antigen, deposition of immune complexes, or lack of immune complex deposition (called pauci-immune glomerulonephritis).

61
Q

CHRONIC (END-STAGE) RENAL DISEASE

• A. Loss of glomeruli and tubules leads to

A

fibrosis.

62
Q

CHRONIC (END-STAGE) RENAL DISEASE: Damaged glomeruli become completely

A

sclerotic (global sclerosis).

63
Q

CHRONIC (END-STAGE) RENAL DISEASE: With advanced loss of tubules and glomeruli, the remaining glomeruli develop

A

adaptive changes. These changes eventually lead to further injury and progressive renal failure.

64
Q

CHRONIC (END-STAGE) RENAL DISEASE: May be detected at routine exam with

A

proteinuria, hypertension or azotemia.

65
Q

CHRONIC (END-STAGE) RENAL DISEASE: Without treatment, ——- prognosis. Renal dialysis and kidney transplantation————- for patient survival

A

POOR, necessary

66
Q

VI. ACUTE PYELONEPHRITIS

A. AKA:
A

tubulointerstitial nephritis.

67
Q

Acute pyelonephritis

A

Suppurative inflammation of kidney and renal pelvis caused by bacterial infection.This is a renal disease affecting tubules, interstitium, and pelvis and is most often secondary to bacterial infection.

68
Q

Acute pyelonephritis: The infection may spread from the

A

urinary bladder, up the ureters and into the renal pelvis and kidney (ascending).

69
Q

Acute pyelonephritis: A second but much less common route in infection is through

A

hematogenous spread of bacteria.

70
Q

ACUTE PYELONEPHRITIS:

  1. Predisposing conditions :
A

Urinary tract obstruction,Instrumentation, Ureteral reflux,Pregnancy, Gender (female), Immunosuppression, Diabetes mellitus

71
Q

ACUTE PYELONEPHRITIS: 2. Clinical:

A

Sudden onset with pain at the costovertebral angle and
systemic evidence of infection. Often there is accompanying dysuria,
frequency and urgency.

72
Q

ACUTE PYELONEPHRITIS: 3. Pathology:

A

Patchy interstitial and tubular neutrophilic inflammation.

73
Q

ACUTE PYELONEPHRITIS: 4. Etiology:

A

Predisposing conditions, include urinary tract obstruction, instrumentation, vesicoureteral reflux, pregnancy, gender and age, diabetes mellitus and immunosuppression.

74
Q

ACUTE PYELONEPHRITIS: 5. Prognosis:

A

Repeated bouts of acute inflammation of continuous inflammation may lead to chronic pyelonephritis. This is characterized by mononuclear inflammatory infiltration and irregular scarring.

75
Q

VII. Drug-Induced Interstitial Nephritis

The etiology includes some

A

antibiotics, non-steroidal anti-inflammatory drugs and others.

76
Q

Drug-Induced Interstitial Nephritis: The pathogenesis involves

A

hypersensitivity reaction to the drugs.

77
Q

DRUG-induced interstitial nephritis: The pathology consists of

A

interstitial infiltration of mononuclear inflammatory cells, often with neutrophils and many eosinophils.

78
Q

Drug-induced interstitial nephritis; Granulomas may be

A

present. The glomeruli are not involved in the inflammation.

79
Q

Drug-induced interstitial nephritis: Large doses of analgesics may lead to

A

interstitial nephritis with papillary necrosis (necrosis of the tips of the medullary pyramids).

80
Q

Drug-induced interstitial nephritis: Treatment: Withdrawal of

A

offending drug and corticosteroids.

81
Q

Drug-induced interstitial nephritis: Prognosis:

A

Generally good with full recovery in 6-8 weeks

82
Q

Acute Tubular Necrosis:

A. Clinical: rapid onset of

A

renal failure, reduced urine output, electrolyte imbalances. The clinical manifestations are reversible over a period of weeks as the damaged tubular epithelium regenerates.

83
Q

Acute Tubular Necrosis: B. Etiology: injury to tubular epithelial cells from

A

ischemia (ie. shock) or a toxin

84
Q

Acute Tubular Necrosis: A. Pathology:

A

dilation of tubules, interstitial edema, necrosis of epithelium (often very focal and subtle with ischemic injury, more diffuse with injury from a toxin)

85
Q

Acute Tubular Necrosis: B. Treatment:

A

Supportive care, dialysis

86
Q

Acute Tubular Necrosis: C. Prognosis: In the absence of preexisting kidney disease, most patients fully recover

A

renal function

87
Q

Arterionephrosclerosis

1. Clinical:

A

Contributing factors are hypertension and diabetes. May
lead to gradual onset of chronic renal failure.

88
Q

Arterionephrosclerosis: 2. Pathology:

A

Gross – kidneys are symmetrically atrophic, with
moderate reduction in size. The kidney surface has an even fine
granularity and the cortex is thin.

89
Q

Arterionephrosclerosis: 3. Histopathology: Narrowing of the lumens of arterioles and arteries
caused by

A

hyaline type of arteriolosclerosis and fibroelastic hyperplasia of muscular arteries. In addition, there is (1) tubular atrophy and interstitial fibrosis and (2) global sclerosis of glomeruli.

90
Q

Arterionephrosclerosis associated with malignant hypertension:
1. Hypertension greater than

A

200/120 mm Hg – occurs in about 5% of

patients with essential hypertension.

91
Q

Arterionephrosclerosis associated with malignant hypertension: 2. Clinical:

A

Relatively rapid onset of renal failure with increased
intracranial pressure leading to headache, nausea, vomiting, and
visual impairment.

92
Q

Arterionephrosclerosis associated with malignant hypertension: 3. Pathology: Arterioles show

A

hyperplastic arteriolosclerosis, reducing

blood flow and causing necrosis of glomeruli.

93
Q

Thrombotic Microangiopathies:

1. Thrombotic thrombocytopenia purpura (TTP) -

A

acquired defect in ADAMTS 13, a plasma protease that degrades vWF multimers. The large von Willebrand factor components activate platelets under certain conditions.

94
Q

Thrombotic Microangiopathies: 2. Hemolytic-uremic syndrome (HUS) -

A

endothelial cell injury which, in most cases, is due to a Shiga-toxin from E. coli (reason for ground beef recalls in the news) or Shigella. The injury leads to platelet activation.

95
Q

Thrombotic Microangiopathies: 3. The pathology is similar in both disorders with

A

microthrombus formation in capillaries.

96
Q

In HUS, renal involvement predominates and the disorder most often occurs in

A

children.

97
Q

There is more widespread involvement of other organs in

A

TTP (Thrombotic thrombocytopenia purpura)

98
Q

Urolithiasis (Renal Stones): • By age 70, affects

A

11% men, 6% women

99
Q

Urolithiasis (Renal Stones): • Clinical: May be

A

asymptomatic, obstruction, intense pain, infection, hematuria
• Types of stones
• Calcium (80%); increased Ca2+ in the urine
• Magnesium ammonium phosphate; alkaline urine, Proteus or staph infection
• Uric acid

100
Q

Urolithiasis (Renal Stones): 1. Clinical: Stones result in

A

urinary tract obstruction, ulceration of the urothelial lining and bleeding.

101
Q

Urolithiasis (Renal Stones): 2. Pathology: Stones are unilateral in

A

80% of patients and most

102
Q

Urolithiasis (Renal Stones): 3. Types of stones

A

calcium
magnesium ammonium phosphate
Uric acid - occur in patients with gout, leukemia (high cell turnover) or
persistently acid urine.

103
Q

Urolithiasis (Renal Stones): 4. Other causes of hydronephrosis -

A

congenital urinary tract
obstructions, enlarged prostate, neoplasms, neurogenic bladder,
pregnancy.

104
Q

Small stones may migrate into the

A

ureters and produce intense flank pain

105
Q

Large stones remain in the

A

pelvis and may be manifested by hematuria and superimposed infection.

106
Q

Stones

may also develop in the

A

bladder.

107
Q

Large stones are referred to as

A

“staghorn calculi”.

108
Q

These large stones form a

A

cast of the pelvis and calyceal system.

109
Q

frequent site for stone formation is within the

A

calyces and pelvis

110
Q

Stone types: calcium -

A

patients have increased concentration of calcium in the urine

111
Q

magnesium ammonium phosphate - patients have

A

persistently alkaline

urine. Infection with Proteus predisposes to these stones.

112
Q

• Uric acid;

A

gout, acid urine, high cell turnover

113
Q

A. Renal Cell Carcinoma

1. Clinical:

A

2:1 male:female ratio. Hematuria, mass, pain, fever,

polycythemia, paraneoplastic syndromes

114
Q

A. Renal Cell Carcinoma: 2. Etiology: Risk factors include

A

smoking, hypertension, obesity,

cadmium exposure and von Hippel-Lindau syndrome.

115
Q

A. Renal Cell Carcinoma: 3. Pathology: Arise from

A

tubular epithelium, often reach a large size

prior to diagnosis, often invade the renal vein.

116
Q

A. Renal Cell Carcinoma: Most common

histologic subtype has cells with very

A

pale or clear cytoplasm (clear cell

carcinoma)

117
Q

A. Renal Cell Carcinoma: 4. Treatment:

A

Surgery +/- radiation

118
Q

A. Renal Cell Carcinoma: 5. Prognosis:

A

Stage dependent 5-yr survival
Stage 1: 81%
Stage 4: 8%

119
Q

A. Renal Cell Carcinoma: 5. Prognosis:

A

Stage dependent 5-yr survival
Stage 1: 81%
Stage 4: 8%

120
Q

B. Wilm’s Tumor

1. Clinical:

A

Abdominal mass, risk is greatly increased in some inherited

syndromes, occurs in children ages 2 to 5 years

121
Q

B. Wilm’s Tumor: 2. Pathology: Triphasic pattern with

A

epithelial structures resembling
primitive tubules or glomeruli, stroma (mesenchymal component) and
blastema which recapitulates early nephron formation.

122
Q

Wilm’s tumor; the tumor
illustrates ——— formation of renal structures in various stages of
renal development.

A

abortive

Perio Exam 2 (20 decks)

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