Infections and Pathology of the Urinary Tract Flashcards

1
Q

Introduction

A

Bacterial infections common in young and
middle-aged females
• Occurs in infant males and elderly men if there
is an underlying UT abnormality
• Aetiologic organisms is usually a gram neg
bacterium, often a faecal contaminant from the
perineum, such as E. coli or Klebsiella
• Basic sequence starts as a cystitis, with or
without vesico-ureteral reflux, followed by
ureteritis and acute pyelonephritis, and possibly
then chronic pyelonephritis

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2
Q

Cystitis:

Introduction/Definition

A
Cystitis
• Inflammation of the urinary bladder,
mostly due to bacterial infection
• Commonly seen in girls and young women
owing to the shorter urethra, as
compared to males
• Cystitis in males is due to an underlying
urethral abnormality
• Congenital urethral valves in infants
• Prostate enlargement in older men
Cystitis
Clinical presentation
• 
Acute cystitis with ulceration
Acute cystitis
A
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3
Q

Cystitis:

Predisposing Factors

A
• Predisposing conditions include:
➢Pregnancy
➢Intercourse with urethral trauma
➢Poor toilet hygiene
➢Diabetes mellitus
➢Instrumentation and catheterization
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4
Q

Cystitis:

Clinical Picture

A
Dysuria
• Frequency
• Nocturia
• Urgency
• Sometimes supra-pubic pain and
tenderness
• Usually no fever
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5
Q

Acute Pyelonephritis:

Definition

A
Defined as infection of the renal pelvis
and parenchyma
• Important cause of renal disease
• Also a commonly undiagnosed cause of
death in diabetic patients
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6
Q

Acute Pyelonephritis:

Pathogenesis

A
Pathogenesis of acute
pyelonephritis
• Ascending infection: starts as an acute
cystitis with damage to the vesicoureteral valves, causing reflux of
infected urine that results in ureteritis
and subsequent pyelitis (inflammation of
the renal pelvis), followed by spread of
infection through collecting tubules into
renal parenchyma
Pathogenesis of acute
pyelonephritis
Pathogenesis of acute
pyelonephritis
• Haematogenous spread from another
infection through septicaemia or pyaemia
• Examples include:
➢Infective endocarditis
➢Pneumonia
➢Osteomyelitis
• Here the infection begins in the renal
parenchyma and then spreads later to the
renal pelvis
• Both kidneys are usually involved
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7
Q

Acute Pyelonephritis:

Clinical Picture

A
Clinical presentation
• Symptoms of cystitis may be present,
i.e. dysuria, frequency, nocturia and
urgency
• Patients are usually febrile
• Flank pain with renal angle tenderness
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8
Q

Acute Pyelonephritis:

Pathology-Macroscopy

A
Pathology of acute pyelonephritis
• Macroscopic appearance:
➢Kidneys are enlarged, red and oedematous
➢Small yellow subcapsular abscesses may be
present
➢Cut-section may show yellow lines of
suppuration stretching up from papillae
➢Pelvic mucosa is hyperaemic and
oedematous
➢Urine is turbid or frankly purulent
Kidney surface with multiple subcapsular abscesses
Abscess within renal parenchyma
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9
Q

Acute Pyelonephritis:

Pathology-Microscopy

A
Pathology of acute pyelonephritis
• Microscopic appearance:
- Neutrophils present within the renal
tubules as well as the interstitium
(infective tubulo-interstitial nephritis)
- May show abscess formation
- Glomeruli are normal
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10
Q

Acute Pyelonephritis:

Complications

A

Acute renal failure
• Recurrent episodes of acute infection with eventual
chronic pyelonephritis
• Papillary necrosis – decrease in medullary blood
flow especially common in diabetic patients or
where there is urinary tract obstruction
• Pyonephrosis whereby pus fills and distends the
entire renal pelvis, calyces and ureter (seen in total
urinary obstruction)
• Rupture of a subcapsular abscess with extension of
infection into the perinephric tissue
• Even septicaemia

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11
Q

Papillary Necrosis

A
Infection in the context of obstruction
• Infection in the context of diabetes
mellitus
• Analgesic nephropathy (NSAID abuse -
phenacetin)
Prognosis of acute pyelonephritis
•
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12
Q

Acute Pyelonephritis:

Prognosis

A
Prognosis is generally good with
antibiotic treatment
• Acute pyelonephritis may prove fatal if
untreated
• Some patients, particularly babies and
elderly individuals, do not necessarily
present with the classic symptoms of
pyelonephritis, so remember to examine
the urine with a dipstick
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13
Q

Chronic Pyelonephritis:

Introduction/Definition

A

Chronic pyelonephritis is fairly common

Usually seen in adults

One of the most common causes of chronic renal failure

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14
Q

Chronic Pyelonephritis:

Aetiology and Pathogenesis

A
• Usually develops as a complication of
repeated attacks of acute pyelonephritis
• Also occurs in chronic urinary tract
obstruction that predisposes to ascending
urinary infections:
➢Calculi (kidney stones)
➢Tumours
➢Prostate enlargement
➢Ureteral strictures
• Congenital vesico-ureteric reflux
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15
Q

Chronic Pyelonephritis:

Vesico-ureter Reflux

A

Vesico-ureteric reflux is a congenital abnormality of the terminal portion of the ureter

Presents in early childhood

The high pressure in the renal pelvis causes intra-parenchymal reflux with parenchymal scarring

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16
Q

Chronic Pyelonephritis:

Pathology-Macroscopic

A
• Macroscopic appearance
➢Unilateral or bilateral involvement
depending on the pathogenesis
➢Kidney is small
➢Kidney shows numerous large, irregular
cortical scars
➢The renal pelvis and calyces are deformed
and often dilated (hydronephrosis) with
accompanying pressure atrophy of renal
cortex
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17
Q

Chronic Pyelonephritis:

Pathology-Microscopic

A

Chronic inflammatory cell infiltrate in the
kidney interstitium, i.e. lymphocytes and
plasma cells

➢Interstitial fibrosis

➢Tubules are atrophic

➢Some tubules are dilated and filled with hyaline casts, which resembles the thyroid gland (called thyroidization)

➢Glomeruli show secondary changes, such as
glomerular sclerosis and peri-glomerular fibrosis

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18
Q

Chronic Pyelonephritis:

Complications

A

Chronic renal failure

Secondary hypertension

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19
Q

Bilharzia:

Incidence

A

All ages

In South Africa, bilharzia is very
common in the provinces north of the
Vaal River, as well as in the northern
regions of Kwa Zulu Natal

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20
Q

Bilharzia:

Pathogenesis

A

Bilharzia caused by the trematode (fluke) Schistosoma haematobium

Bilharzia seen where fresh water has become contaminated by Schistosoma

People bathing or swimming in such water are at risk

Lifecycle involves the fresh water snail and the human

Schistosoma ova (eggs) are excreted in the urine into the water

Ovum releases a motile ciliated miracidium that enters an aquatic snail host

After a period of development within the snail
host, the cercaria are released, and these penetrate the skin of people in the water

The cercaria, now called schistosomules,
migrate to the lungs where they mature into adult worms

Adult worms usually migrate to the portal vessels where they mate

The adult female fluke then migrates to the venous plexus around the bladder

The ova (eggs) are laid in the bladder wall

The eggs secrete enzymes that dissolve host
tissues in the vicinity, and so doing allows the
eggs to enter the bladder lumen, where they
can be excreted in the urine, and so perpetuate
the cycle

Live bilharzia eggs elicit an acute inflammatory
reaction

Once the eggs die and calcify, they elicit a
granulomatous response as well as fibrosis

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21
Q

Bilharzia:

Clinical Presentation

A

The most important clinical feature in bilharzial cystitis is haematuria

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22
Q

Bilharzia:

Pathology-Macroscopy

A

Mucosa of the bladder and ureters becomes thickened and granular, i.e. a ‘wet sand’ appearance macroscopically

Ureters may become stenotic because of
the fibrosis

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23
Q

Bilharzia:

Pathology-Microscopy

A

Bilharzia ova present in mucosa, viable or
calcified

Acute inflammation with eosinophils

Granulomas with foreign body-type giant cells

Later fibrosis

Overlying transitional epithelium undergoes
squamous metaplasia

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24
Q

Bilharzia:

Complications

A

• Squamous cell carcinoma of bladder
• Fibrosis of ureter(s) causes ureter
obstruction, which leads to hydronephrosis
and predisposes to ascending bacterial
infections of the urinary tract, such as
pyelonephritis
• In a heavy Schistosoma infestation, eggs
may enter the systemic venous circulation,
i.e. vesical venous plexus to inferior vena
cava, and so embolise to the lungs, causing
pulmonary hypertension

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25
Q

Renal Tuberculosis

A

Uncommon

Secondary to pulmonary tuberculosis

Two types:
1.Miliary tuberculosis

2.Isolated organ tuberculosis, called
tuberculous pyelonephritis, which may be
uni- or bilateral, and shows extensive
caseation and destruction of the kidney

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26
Q

Glomerular Disease/Glomerulopathy:

Definition/Introduction

A

The term glomerulopathy includes several diseases that affect the glomeruli (inflammatory and non-inflammatory)

Glomerulonephritis refers to inflammatory disease /
inflammation of the glomerulus.

These diseases have different aetiologies, different
morphologic appearances and varying prognoses

The glomerulopathies may also clinically present in
different ways

Some glomerulopathies resolve and have a good prognosis, but other cases follow a chronic course, resulting in a chronic glomerulonephritis /-opathy with eventual chronic renal failure (such patients require dialysis and/or renal transplantation)

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27
Q

Glomerular Disease/Glomerulopathy:

Aetiology

A
  1. Primary, i.e. the glomeruli are the primary target of the disease process
  2. Secondary, i.e. glomerular damage occurs because of another underlying systemic disease (extra-renal organs also involved):
    - Autoimmune diseases, like SLE (inflammatory)
    - Diabetes mellitus (non-inflammatory)
    - Systemic hypertension (non-inflammatory)
28
Q

Glomerular Disease/Glomerulopathy:

Clinical Presentation

A

Recurrent painless haematuria

Asymptomatic proteinuria

Nephritic syndrome:
➢ Haematuria
➢ Proteinuria
➢ Hypertension

Nephrotic syndrome:
➢ Heavy proteinuria (in adults >3,5 g/day and in children >2 g/m²/day)
➢ Hypoproteinaemia
➢ Severe oedema (often anasarca)
➢ Hypercholesterolaemia

Chronic renal failure
Acute diffuse proliferative
glomerulonephritis
• Incidence:
➢ Fairly common
➢ All age groups, but mainly children
• Aetiology:
➢ Usually follows on a streptococcal infection (often
called post streptococcal glomerulonephritis)
• Pathogenesis:
➢ Antibodies bind to the organism, complement is bound
and immune complexes are formed, which are deposited
on the subepithelial part of the glomerular basement
membrane
• Clinical picture:
➢ Nephritic syndrome

29
Q

Glomerular Disease/Glomerulopathy:

Clinical Presentation

A

Recurrent painless haematuria

Asymptomatic proteinuria

Nephritic syndrome:
➢ Haematuria
➢ Proteinuria
➢ Hypertension

Nephrotic syndrome:
➢ Heavy proteinuria (in adults >3,5 g/day and in children >2 g/m²/day)
➢ Hypoproteinaemia
➢ Severe oedema (often anasarca)
➢ Hypercholesterolaemia

Chronic renal failure

30
Q

Acute Diffuse Proliferative Glomerulonephritis:

Incidence

A

Fairly common

All age groups, but mainly children

31
Q

Acute Diffuse Proliferative Glomerulonephritis:

Aetiology

A

Usually follows on a streptococcal infection (often

called post streptococcal glomerulonephritis)

32
Q

Acute Diffuse Proliferative Glomerulonephritis:

Pathogenesis

A

Antibodies bind to the organism, complement is bound and immune complexes are formed, which are deposited on the subepithelial part of the glomerular basement membrane

33
Q

Acute Diffuse Proliferative Glomerulonephritis:

Clinical Picture

A

Nephritic syndrome

34
Q

Acute Diffuse Proliferative Glomerulonephritis:

Pathology-Macroscopy

A

Kidneys slightly enlarged

Pale appearance

35
Q

Acute Diffuse Proliferative Glomerulonephritis:

Pathology-Microscopy

A

All glomeruli involved, i.e. diffuse

The entire glomerulus is involved, i.e. global

Glomeruli are hypercellular owing to increase in
mesangial cells and swelling of endothelial cells

Glomeruli have a lobular appearance

Neutrophils in glomeruli

Tubules contain casts and may show acute tubular
necrosis

36
Q

Acute Diffuse Proliferative Glomerulonephritis:

Pathology-Ultrastructural

A

Immune complexes are present between the podocytes (visceral epithelial cells) and the glomerular basement membrane, forming so-called “subepithelial humps”

37
Q

Acute Diffuse Proliferative Glomerulonephritis:

Prognosis

A

In children, prognosis is good, with over 90% of patients recovering within weeks

In adults, prognosis is reasonable, with
approximately 60% of patients recovering

Death may occur

Hypertension in the acute phase

More commonly, death results from progressive renal disease and chronic renal failure

38
Q

Membranous Glomerulopathy:

Incidence

A

Less common than post streptococcal
glomerulonephritis, but still fairly common

All age groups, but usually adults

39
Q

Membranous Glomerulopathy:

Aetiology

A

Primary (85% of cases)

Secondary (15% of cases), which includes:
~ Infections, e.g. hepatitis B, syphilis, malaria
~ Drugs (penicillamine, gold, mercury, heroin)
~ Certain malignant tumours (lymphomas, melanomas, bronchus and breast CA)

40
Q

Membranous Glomerulopathy:

Pathogenesis

A

Immune complexes are formed and deposited between the basement membrane and the epithelial cells

The basement membrane then grows outwards
so that the immune complexes are eventually
incorporated into the basement membrane

41
Q

Membranous Glomerulopathy:

Clinical Picture

A

Initially nephrotic syndrome, but some patients

progress to chronic renal failure

42
Q

Membranous Glomerulopathy:

Pathology-Microscopy

A

➢The glomerular basement membrane shows
diffuse thickening, giving a rigid appearance to
the glomerulus on light microscopy (i.e. open
loops but with thickened walls)
➢No increase in cellularity
➢No inflammatory cells either
➢Silver stains accentuate the thickened
basement membranes, showing characteristic
“spikes”

43
Q

Membranous Glomerulopathy:

Pathology-Ultrastructure

A
The electron microscopic picture varies
according to the stage of the disease:
➢Stage I: Subepithelial immune complex
deposits (these deposits are actually
intramembranous)
➢Stage II: Deposits and BM “spikes”
➢Stage III: Deposits enclosed by BM
➢Stage IV: Deposits disappear, with a
“moth-eaten” appearance to the basement
membrane
44
Q

Membranous Glomerulopathy:

Prognosis

A

In children, prognosis is reasonable

In adults, prognosis is less favorable

Prognosis remains unpredictable

45
Q

Minimal Change Disease:

Incidence

A

Fairly common

Mainly children aged 1 to 4 years of age

46
Q

Minimal Change Disease:

Aetiology

A

Unknown

47
Q

Minimal Change Disease:

Pathogenesis

A

There is damage to the glomerular basement
membrane causing a selective proteinuria of low
molecular weight protein, such as albumin

No immune complex formation (no inflammation)

48
Q

Minimal Change Disease:

Clinical Picture

A

Nephrotic syndrome

49
Q

Minimal Change Disease:

Pathology-Microscopy

A

Normal

50
Q

Minimal Change Disease:

Pathology-Ultrastructure

A

Shortening and fusion of the foot processes of the podocytes (this is nonspecific and probably results from the proteinuria)

Prominent microvilli

51
Q

Minimal Change Disease:

Prognosis

A

Generally good

Patients usually respond dramatically to
steroid therapy

52
Q

Rapidly Progressive Glomerulonephritis:

Incidence

Aetiology

A

Rare

Aetiology:

Commonly follows on post streptococcal glomerulonephritis but it can also complicate other types of glomerulonephritis
(eg. SLE, vasculitides)

Also known as CRESCENTIC GLOMERULONEPHRITIS

53
Q

Rapidly Progressive Glomerulonephritis:

Pathogenesis

A

There is severe glomerular injury causing leakage of fibrin, which in turn stimulates the epithelial cells lining Bowman’s capsule to proliferate

These cells form “crescents” which eventually compress the glomeruli

54
Q

Rapidly Progressive Glomerulonephritis:

Pathology-Microscopy of crescentic
glomerulonephritis

A

Usually an acute diffuse proliferative
glomerulonephritis is present

Formation of cellular crescents

Cellular crescents eventually become
fibrotic crescents

55
Q

Rapidly Progressive Glomerulonephritis:

Prognosis

A
Prognosis is very poor
• Crescentic glomerulonephritis is
characterised by a rapid clinical course,
hence its alternative name of rapidly
progressive glomerulonephritis
• Patients die of chronic renal failure
within months
56
Q

Diabetes Mellitus:

Incidence

A

Diabetes mellitus is a frequent cause of renal disease, particularly in type I diabetes (IDDM)

57
Q

Diabetes Mellitus:

Pathogenesis

A

Microangiopathy

58
Q

Diabetes Mellitus:

Clinical Presentation

A

Initially nephrotic syndrome

Later hypertension and chronic renal failure

59
Q

Renal Pathology of Diabetes Mellitus

A

Diffuse glomerulosclerosis:

➢Diffuse increase in the amount of the
mesangial matrix and thickened basement
membrane

Nodular glomerulosclerosis:

➢Nodular lesions of mesangial matrix present in some of the glomeruli

Insudative lesions (comprise of plasma proteins and lipid):

➢Hyaline arteriolosclerosis, i.e. hyaline thickening of the small arteries and arterioles

➢“Capsular drop” within the basement membrane of Bowman’s capsule

➢“Fibrin cap” around the periphery of the glomerular capillary loops

60
Q

Diabetes Mellitus:

Complications

A

Increased incidence of urinary tract infections

More susceptible to papillary necrosis in acute pyelonephritis

61
Q

Focal Segmental Glomerulosclerosis:

Incidence

A

Important cause of nephrotic syndrome

10 % of nephrotic syndrome in children

Primary or secondary to other disease causing focal segmental scarring of the glomerulus:

➢Diabetes, HIV, heroin abuse, reflux

62
Q

Focal Segmental Glomerulosclerosis:

Pathogenesis

A

Focal (some of the glomeruli) segmental (only

part of the glomerulus) is scarred (sclerotic)

63
Q

Acute Tubular Necrosis:

Aetiology

A

Important cause of renal failure

Toxic injury (drugs or toxins) or

Ischaemic injury (usually secondary to haemodynamic causes eg. shock)

64
Q

Acute Tubular Necrosis:

Clinical Picture

A

Oliguric phase followed by diuretic phase

Regeneration of the tubules permits clinical recovery

65
Q

Acute Tubular Necrosis:

Pathology-Macroscopic

A

Pale cortex

Swollen medulla

66
Q

Acute Tubular Necrosis:

Pathology-Microscopic

A

Tubular epithelial cell injury (no glomerular

involvement) :
- No proteinuria
- Only abn in electrolyte and fluid homeostasis

Sloughing to form cellular and granular casts

Vacuolisation of cells

Flattening of cells