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General Pathology > Urinary System > Flashcards

Urinary System Flashcards

1
Q

What does the kidney excrete?

A
  • urea (end product of protein metabolism)
  • uric acid (end product of purine and pyrimidine metabolism)
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2
Q

What does the kidney regulate?

A
  • electrolytes and minerals (Na, K, Ca, P)
  • blood pressure
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3
Q

What does the kidney secrete?

A
  • erythropoietin
  • active form of vitamin D
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4
Q

The kidney eliminates ______, conserves _____, and maintains ______

A
  • solutes
  • protein
  • pH
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5
Q

What are the four main parts of the kidney affected by disease? What is each part most often affected by?

A
  • Glomeruli: immunologic diseases
  • Tubules: often affected by toxic/infectious agents
  • Interstitium: often affected by toxic/infectious agents
  • Blood vessels
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6
Q

What are interdependent parts in relation to the kidney?

A
  • effects on one often effect all the others.
  • Chronic renal diseases eventually tend to damage all 4 parts which can lead to end stage kidney disease.
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7
Q

What are important components of the glomerulus?

A
  • Bowman’s space
  • fenestrated endothelium (70-100nm space)
  • glomerular basement membrane
  • Podocytes
  • mesangial cells support
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8
Q

What is bowman’s space?

A

(urinary space)
lined by parietal epithelium on outside and visceral epithelium (podocytes) on the inside

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9
Q

What is the Glomerular basement membrane (GBM) made of?

A

mostly made of Type IV collagen

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10
Q

What are podocytes separated by?

A

20-30nm filtrations slits, bridged by a slit diaphragm made of nephrin

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11
Q

In regards to kidney filtration, it is highly permeable to what? It is impermeable to what?

A

Highly permeable:
- water
- small

Impermeable
- large molecules/proteins

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12
Q

What does the filtration slit diaphragm do?

A
  • prevents backflow of water
  • normally a diffusion barrier for proteins (loss leads to protein leakage = nephrotic syndrome)
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13
Q

What are key clinical changes in renal disease?

A
  • azotemia
  • uremia
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14
Q

What is azotemia?

A

↑ blood urea nitrogen (BUN) and creatinine, often due to ↓ glomerular filtration rate (GFR)

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15
Q

What is uremia?

A

progression of azotemia to clinical level with failure of renal excretory function and systemic problems

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16
Q

What are secondary effects of uremia?

A

► GI - gastroenteritis
► Neuromuscular - peripheral neuropathy
► Cardiovascular - pericarditis
► Oral - severe ulcers

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17
Q

What is Glomerulonephritis

A

There is inflammation, mesangial and/or basement membrane thickening which causes barrier dysfunction.

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18
Q

What are the 2 major clinical presentations of Glomerulonephritis

A

–nephrotic syndrome

–nephritic syndrome

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19
Q

What is the pathogenesis of nephrotic syndrome?

A

Alteration of glomerular capillary walls causing permeability to plasma proteins

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20
Q

What are some clinical results of nephrotic syndrome?

A
  • Massive proteinuria (≥3.5gm/day)
  • Hypoalbuminemia (plasma albumin <3gm/dL
  • Generalized edema
  • Hyperlipidemia and lipiduria
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21
Q

In nephrotic syndrome, what happens when there is glomerular capillary leakage of albumin?

A

It leads to hypoalbuminemia → hyperlipidemia or anasacra

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22
Q

In nephrotic syndrome, what happens when there is glomerular capillary leakage of water and sodium?

A

Leads to ADH and aldosterone production → water and Na retention → anasarca

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23
Q

In nephrotic syndrome, what happens when there is glomerular capillary leakage of immunoglobulin or complement?

A

leads to staph infection and pneumonia

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24
Q

In nephrotic syndrome, what happens when there is glomerular capillary leakage of anticoagulants?

A

Leads to hypercoagulability → thrombosis and thromboembolism

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25
Q

Understand what can happen after glomerular capillary leakage in nephrotic syndrome

A

(See chart on slide 17)

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26
Q

What is the pathogenesis of nephritic syndrome?

A

Inflammatory (leukocytic) reaction injures glomerular capillaries, allows escape of RBCs into urine and leads to ↓GFR

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27
Q

What are signs and symptoms of nephritic syndrome?

A
  • Hematuria with dysmorphic RBCs
  • ↓GFR, oliguria (↓urination), and azotemia (↑BUN)
  • Hypertension- due to renin release
  • Mild proteinuria/edema: not as severe as nephrotic syndrome
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28
Q

Glomerulonephritis causes are most often ________

A
  • immune-mediated

(antibody or immunocomplex formation)

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29
Q

What causes primary glomerulonephritis?

A

(kidney is only or predominant organ): Many won’t discuss

  • Post-streptococcal glomerulonephritis: nephritic syndrome
  • Acute postinfectious glomerulonephritis
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30
Q

What causes secondary glomerulonephritis?

A

(systemic disease leads to glomerular damage)

  • hypertension
  • diabetes: nephrotic syn.
  • amyloidosis: nephrotic syn.
  • lupus erythematosus: nephrotic or nephritic syn.
  • Goodpasture sx
  • granulomatosis with polyangiitis (GPA)
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31
Q

What is Post-streptococcal GN

A
  • antibody bound to strep. proteins (immune complexes) causes proliferation of glomerular cells and activates complement which leads to infiltration of leukocytes (especially neutrophils)
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32
Q

In Post-streptococcal GN, you may have nephritic syndrome with gross ______ (smoky brown)

A

hematuria (urine in blood)

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33
Q

In post-streptococcal GN, what is the outcome for kids? Adults?

A

-Most kids recover completely
-In adults, 15-50% develop end-stage renal disease over years to decades

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34
Q

What is the Glomerulonephritis Immune Injury mechanism

A

► Deposition of circulating antigen/antibody complexes deposited in the glomerulus (type III hypersensitivity)

► Antibodies binding to glomerular antigens or molecules planted in the glomerulus (type II hypersensitivity)

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35
Q

What are examples of the injury mechanism:
deposition of circulating antigen/antibody complexes deposited in the glomerulus (type III hypersensitivity)

A
  • Lupus
  • Poststreptococcal
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36
Q

What are examples of the injury mechanism:
Antibodies binding to glomerular antigens or molecules planted in the glomerulus (type II hypersensitivity)

A
  • Goodpasture sx: kidney and lung lesions
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37
Q

In Glomerulonephritis immune injury mechanism, Antigen/Antibody complexes (circulating or in-situ) activate what?

A
  • complement
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38
Q

What happens when complement is activated in the immune injury mechanism of GN?

A
  • C5a → recruits neutrophils and MACs
  • also stimulates TGF-β production by podocytes → increased synthesis of extracellular matrix → GBM thickening
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39
Q

What do the neutrophiles release in the immune injury mechanism of GN? What is the result of each?

A
  • Proteases → GBM degradation
  • Free radicals → cell damage
  • Arachidonic acid metabolites → ↓GFR
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40
Q

What is the end result of immune injury mechanism of GN?

A

Glomerular damage (whether to the endothelium, basement membrane or podocytes) → loss of barrier function → proteinuria and sometimes ↓GFR

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41
Q

How do you diagnose Glomerulonephritis

A

► Urinalysis - nephrotic syn., nephritic syn. or other
► Serology (blooddraw) - circulating autoantibodies
► Renal Biopsies (light microscopy, (immuno)fluorescence microscopy (no deposits, linear or granular), electron microscopy rarely))

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42
Q

What is Direct immunofluorescence (DIF) testing?

A

tests patient tissue directly for presence of autoantibodies

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43
Q

What is Indirect immunofluorescence (IIF)

A
  • tests patient’s blood for presence of autoantibodies in: HEp-2 cell lines, Specific tissues, & Granulocytes
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44
Q

What are HEp-2 cell lines in indirect immunofluorescence

A

useful for wide range of antinuclear antibodies (ANA) and cytoplasmic components

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45
Q

What are Specific tissues in indirect immunofluorescence?

A

(e.g. skin, oral epithelium)- use a similar animal epithelium (i.e. monkey/rat) as a substrate

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46
Q

What are granulocytes in indirect immunofluorescence?

A

ANCA = anti-neutrophil cytoplasmic antibodies.

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47
Q

What are the different Indirect Immunofluorescence ANA Staining Patterns

A

Negative, nuclear, cytoplasmic, mitotic

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48
Q

What are the different Indirect Immunofluorescence antineutrophil cytoplasmic antibodies (ANCA) Staining Patterns

A

ANCA primarily involves antibodies that display perinuclear (pANCA) or cytoplasmic (cANCA) staining

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49
Q

What is Glomerular Injury, Non-immune-mediated

A
  • Mutations in slit diaphragm (e.g. nephrin)
  • Nephron Loss (due to any disease)
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50
Q

How does nephron loss cause non immune mediated glomerular injury?

A

When GFR is reduced to 30-50% of normal function →
triggers remaining glomeruli to hypertrophy to compensate →
increases single nephron GFR and glomerular blood pressure →
causes endothelial and epithelial injury →
more proteinuria, matrix production →
progression to end stage renal disease usually occurs with proteinuria and global glomerulosclerosis

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51
Q

What is Tubulointerstitial Nephritis (TIN)

A
  • Most forms of tubular injury also involve the interstitium
  • Caused by either bacteria or non-bacterial etiologies
52
Q

What are the bacteria/non-bacteria etiologies of Tubulointerstitial Nephritis (TIN)

A
  • Bacteria (Pyelonephritis)

– Non-bacterial cause (Interstitial nephritis): due to drugs, metabolic disorders, physical injury, viral infections, immune reactions

53
Q

What is acute pyelonephritis

A

Common manifestation of extension from a lower urinary tract infection (bladder usually involved)

54
Q

What causes Acute Pyelonephritis?

A
  • Gram Negative bacteria (most often E. Coli)
55
Q

How does Acute Pyelonephritis spread?

A
  • ascending infection (most common)
  • hematogenous (e.g. septicemia)
56
Q

Why is Acute Pyelonephritis more common in females?

A
  • shorter urethra
  • close proximity to anus
  • pregnancy (20-40% develop UTI)
57
Q

What are predisposing factors for Acute Pyelonephritis (5)

A
  • Urinary obstruction (BPH in males or renal lesions) or bladder dysfunction leads to stasis favoring bacterial growth
  • Instrumentation of urinary tract (catheterization)
  • Vesicoureteral reflux
  • Diabetes mellitus: ↑ susceptibility to infection and neurogenic bladder dysfunction
  • Immunosuppression and immunodeficiency
58
Q

What are clinical features of Acute Pyelonephritis (5)

A

► abrupt onset of costovertebral angle pain
► systemic signs of infection (fever, chills, malaise)
► nausea/vomiting
► pyuria, bacteriuria
► urethral irritation (dysuria, increased frequency and urgency)

59
Q

In Acute Pyelonephritis, how long do symptoms usually last without tx?

A

Symptoms usually last 1 week without tx. It is usually unilateral so renal failure does not occur

60
Q

Describe the histology of Acute Pyelonephritis

A
  • Patchy neutrophilic infiltration of interstitium. Glomeruli intact; tubules spread apart and necrotic.
  • Collecting tubules filled with pus, passes out in the urine.
61
Q

Chronic Pyelonephritis (either related to obstruction or vesicoureteral reflux) damages what?

A

Damages tubules, calyces, and pelvis leading to scarring

62
Q

Chronic Pyelonephritis may be asymptomatic until….

A

Polyuria (can’t concentrate urine) and resulting hypertension and renal failure (if bilateral) occur and/or routine urinalysis shows WBC’s

63
Q

What does Interstitial Nephritis refer to?

A

► Refers to scarring, atrophy, inflammation around tubules. Typically refers to a non-bacterial cause

64
Q

What is drug-induced interstitial nephritis

A
  • IgE or T cell mediated immune reaction to a drug (methicillin, ampicillin, diuretics, NSAIDS)
  • interstitial mononuclear inflammation with eosinophils
65
Q

What is acute tubular injury (ATI)

A

Clinicopathologic entity - damaged tubular epithelial cells with acute decline of renal function (decreased GFR)

66
Q

What is the most common cause of acute kidney injury (renal failure)

A

Acute Tubular Injury (ATI)

67
Q

What are the two patterns of Acute Tubular Injury (ATI)

A
  • ischemic
  • Nephrotoxic
68
Q

When does ischemic Acute Tubular Injury (ATI) occur

A

occurs when marked decrease in blood flow to kidney (trauma, acute pancreatitis, or septicemia leading to shock)

69
Q

When does nephrotoxic Acute Tubular Injury (ATI) occur

A
  • exposure to toxins: poison
  • heavy metals
  • drugs: antibiotics
70
Q

What is the pathogenesis of Acute Tubular Injury (ATI)

A
  • ischemia or toxic injury causes tubule cells to be shed (casts seen in urine). This blocks urine output, increases interstitial pressure and decreases GFR
  • Oliguria leads to uremia
71
Q

What is the outcome of Acute Tubular Injury (ATI)

A
  • Reversible when caught early–death is circumvented thru dialysis and maintaining electrolytes
  • Final complete recovery (>90%)
72
Q

What is the onset of Acute Kidney Injury (Acute Renal Failure)

A

Abrupt onset (within 48 hrs) of renal dysfunction

73
Q

What are signs and symptoms of Acute Kidney Injury (Acute Renal Failure)

A
  • Increased serum creatinine
  • Oligouria or anuria
  • Azotemia
74
Q

What are the causes of Acute Kidney Injury (Acute Renal Failure)

A
  • Prerenal: decreased blood flow to kidneys (e.g. cardiac failure)

– Intrarenal: ATI is most common cause but also acute glomerular, interstitial or vascular disease

– Postrenal: obstruction of urinary tract distal to the kidney

75
Q

What are signs and symptoms of Chronic Kidney Injury (Chronic Renal failure)

A
  • Azotemia slowly progressing to uremia which causes oral ulcers, gastroenteritis, pericarditis, peripheral neuropathy
  • hypertension
  • some degree of proteinuria
76
Q

What can Chronic Kidney Injury (Chronic Renal failure) cause?

A

All chronic kidney diseases can cause severe progressive scarring leading to end stage kidney disease (ESRD)

77
Q

What are some examples of renal vascular diseases?

A
  • Benign nephrosclerosis
  • Malignant hypertension/malignant nephrosclerosis
  • Thrombotic microangiopathies
78
Q

What is another name for Arterionephrosclerosis

A

Benign Nephrosclerosis

79
Q

What is Arterionephrosclerosis

A

Thickening, luminal obstruction of arteries and arterioles most often associated with benign hypertension and diabetes

80
Q

What does Arterionephrosclerosis cause?

A

Causes parenchymal ischemia resulting in small foci of parenchymal loss and fibrosis

81
Q

What is the kidney like in Arterionephrosclerosis? The small vessels?

A
  • Kidney is small and contracted with a grain leather surface
  • Small vessels show hyaline deposition (arteriolosclerosis), thickened wall with narrowed lumen
82
Q

What is malignant hypertension? Is it common or not?

A
  • Blood pressure usually > 200/120 mmHg
  • Uncommon, 5% of patients with hypertension, or may also arise de novo
83
Q

What are symptoms of malignant hypertension?

A
  • Increased intracranial pressure→ headache, nausea, vomiting, visual impairment
  • Proteinuria, hematuria
  • Renal failure arises later
84
Q

What is the outcome if someone has malignant hypertension?

A
  • Medical emergency requiring aggressive antihypertensive therapy
  • 50% survive 5 yrs
85
Q

What is the pathogenesis of malignant hypertension?

A

Long-standing hypertension →

vascular damage →

narrows lumen of the afferent arteriole →

ischemia →

↑ renin →

angiotensin II →

vasoconstriction →

↑↑ renin →

↑↑ blood pressure

86
Q

What are general traits of cystic diseases of the kidney?

A
  • Common; may be inherited, developmental or acquired
  • can be confused with malignant tumors
  • Adult polycystic kidney disease: a major cause of renal failure
87
Q

How are simple cysts found in the kidney?

A
  • Single or multiple
  • Variably sized (1-5 cm)
  • Usually in cortex
  • Features that are different from tumors (Smooth contours, avascular, fluid filled)
88
Q

Describe Dialysis-associated acquired cysts

A

– In cortex and medulla

– May bleed leading to hematuria

– Tumors may arise in them

89
Q

What is Adult Polycystic Kidney Disease

A
  • A common autosomal dominant condition
  • Normal at birth, both kidneys progressively develop multiple enlarging cysts that destroy parenchyma
90
Q

When do signs and symptoms of Adult Polycystic Kidney Disease arise? What are they?

A

symptoms develop in the 4th decade:

  • hematuria
  • flank pain
  • hypertension
  • polyuria
  • kidney enlargement
91
Q

What is the outcome of Adult Polycystic Kidney Disease

A
  • Eventual renal failure by age 50-70
  • Ultimately fatal due to hypertension or uremia
92
Q

Why are tubular precipitations bad?

A

Can obstruct/damage the tubules and hinder renal function

93
Q

What are the different types/causes of tubular precipitations

A
  1. Urolithiasis (Urinary tract stones): a variety of types (discuss next)
  2. Multiple myeloma
    - Bence-Jones casts in tubules
    - Hypercalcemia
    - Amyloidosis
    - tumor deposits
94
Q

What is Nephrocalcinosis

A

Increased calcium content in the tubules and interstitium due to hypercalcemia

95
Q

When does Nephrocalcinosis cause dysfunction

A

Generally do not cause dysfunction unless massive

96
Q

What are Urolithiasis/nephrolithiasis (Kidney Stones)

A

Precipitations of a variety of different compounds due to increased urinary concentration of the stone’s components (supersaturation)

97
Q

What are effects of Urolithiasis/nephrolithiasis (Kidney Stones)

A

– Large stones collect in the calyces. May remain silent or cause obstruction with hematuria

– Small stones lodge in ureters where they cause intense renal colic (excruciating flank pain), ulceration and hematuria

– Both large and small stones predispose to infection

98
Q

What is treatment for Urolithiasis/nephrolithiasis (Kidney Stones)

A
  • Surgery
  • chemical dissolution
  • ultrasound lithotripsy
99
Q

What makes up Kidney Stones (urolithiasis)

A

Calcium Oxalate and/or Calcium Phosphate (80% of cases)

100
Q

What is the cause of Kidney Stones (urolithiasis)

A

Cause is not always clear, usually high urine levels of components (Hypercalciuria & Hyperoxaluria)

101
Q

What is Hypercalciuria in relation to kidney stones?

A

overabsorption from gut or renal reabsorption defect. Can also be caused by hypercalcemia due to:

  • Hyperparathyroidism
  • Myeloma, sarcoidosis, bone destroying tumors
  • Overdose of calcium or vitamin D in diet
102
Q

What is Hyperoxaluria in relation to kidney stones?

A

can lead to oxalosis (deposits in other tissues). From eating rhubarb leaves (and other plants), antifreeze or from general anesthesia

103
Q

What is Obstructive Uropathy

A

If ureters, calyces or urethra are obstructed, urine backs up and causes infection of kidney (pyelonephritis) or pressure atrophy of renal parenchyma (hydronephrosis)

104
Q

What are causes of Obstructive Uropathy

A
  • Congenital or secondary strictures
  • Kidney stones
  • Prostate enlargement
  • Tumors
  • Bladder atony
105
Q

What are symptoms of Obstructive Uropathy

A
  • Bilateral hydronephrosis causes anuria and can be quickly corrected
  • Unilateral hydronephrosis is asymptomatic and causes loss of renal function. This is unfortunate because if it caused symptoms it could be corrected.
106
Q

What is a renal adenoma?

A

Benign tumor of tubular epithelium

107
Q

How do renal adenomas appear?

A

Grossly appear as well demarcated yellow, lipid filled nodules in the upper pole of the cortex and measuring < 2.5 cm

108
Q

How should renal adenomas be treated?

A

No reliable way to differentiate them from kidney cancers so all should be treated as if it could be cancer

109
Q

What is renal cell carcinoma?

A

Malignant tumor of renal tubular cells resembling the adenoma grossly and histologically but are larger (> 3 cm)

110
Q

What are signs and symptoms of Renal Cell Carcinoma

A

– Dull flank pain

– palpable abdominal mass

– Painless hematuria (most common symptom)

– Polycythemia

– tumor makes erythropoietin

111
Q

What is the outcome of renal cell carcinoma?

A
  • Spreads to lung, bone
  • Unpredictable course; usually fatal
112
Q

What is Wilms Tumor?

A

► One of the common childhood malignancies

► Unilateral or bilateral kidney tumor derived from embryonic rests

113
Q

Wilms Tumor is associated with ______

A

syndromes

114
Q

How does Wilms Tumor present?

A

Present as large, painful abdominal masses with lung metastasis

115
Q

What is the outcome of Wilms Tumor

A

90% survival with nephrectomy and chemotherapy

116
Q

What is Cystitis

A

inflammation of the bladder

117
Q

What causes Cystitis

A

► Infection with coliforms (gram neg. rods):
- Women are predisposed because of short urethras and trauma from sex
- Diabetes
- Catheterization
- Urinary retention or obstruction from hypotonic bladder, prostate enlargement
► Radiation, chemotherapy, immunosuppression

118
Q

What are symptoms of Cystitis

A
  • Urinary frequency
  • Suprapubic pain
  • Dysuria (pain or burning on urination)
119
Q

What does cystitis predispose you to

A

predisposes to ascending kidney infection

120
Q

What are risk factors of Transitional Cell (Urothelial) Carcinoma (Bladder Cancer)

A
  • Cigarette smoking: excreted carcinogens in cigarette smoke
  • Industrial exposure to aniline dyes
  • Long term use of analgesics (aspirin with phenacetin)
  • Previous radiation or chemotherapy
121
Q

What does Transitional Cell (Urothelial) Carcinoma (Bladder Cancer) start as?

A

Typically starts as a papillary non-invasive tumor that causes painless hematuria

122
Q

What is the difference in low grade and high grade transitional cell (Urothelial) carcinoma (Bladder Cancer)

A
  • Low grade examples are slow to invade; high grade tumors are already invasive on discovery in 80%
  • Low grade tumors tend to recur but have a 98% survival
123
Q

What is the prognosis for transitional cell (Urothelial) carcinoma (Bladder Cancer) when it invades the muscle?

A

Once they invade muscle, prognosis is 50%

124
Q

What causes bladder obstruction

A
  • Prostate cancer, prostatitis or BPH
  • Urethral strictures
125
Q

What is the pathology of bladder obstruction

A

– Bladder becomes distended in acute obstruction

– In partial chronic obstruction, muscular hypertrophy develops and causes a thickened, trabeculated muscular wall

– if left untreated can affect the kidney

General Pathology (32 decks)

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