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MD3002 > Pathology of the Kidney, Ureters and Bladder 1 > Flashcards

Pathology of the Kidney, Ureters and Bladder 1 Flashcards

1
Q

Identify the main kinds of pathologies which can occur to the kidney.

A

• Trauma

• Tumor
– Non-neoplastic
– Benign
– Malignant (primary or secondary)

• Chronic
– Chronic inflammatory

• Acute
– Infection
– Acute inflammation
– Immunological

• Stone
– Genetic
– Metabolic

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2
Q

Identify urinary causes of heamaturia.

A

UTIs
Kidney stones
Bladder cancer

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3
Q

Identify urinary causes of acute renal failure.

A
  • Pre-renal (Transient renal hypoperfusion due to hypotension, reduced CO)
  • Renal (toxic insult, glomerulonephritis, Acute tubular necrosis)
  • Post-renal (ureter stone)
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4
Q

Identify urinary causes of proteinuria.

A
  • Glomerulonephritis (damaged filter)
  • Hypertension (high flow damages glomerular capillaries)
  • Diabetes (damaged filter)
  • Infection (and possibly inflammation leading to exudate-
  • Renal stone (can cause inflammation and therefore exudate)
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5
Q

Define renal failure. What are the consequences of this ?

A

Inability of the kidney to maintain normal function, so cannot maintain:
• Fluid and electrolyte balance
• Resorption of solutes
• Excretion (eg of conjugated xenobiotics)
• Endocrine role
– Renin
– Erythropoietin

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6
Q

Distinguish between congenital and genetic disease.

A

Congenital means present at birth
Genetic means it has a genetic component

“Generally speaking, a lot of genetic diseases do manifest at birth and thus are congenital. On the other hand, a lot of congenital diseases are hereditary or have a significant genetic factor. All genetic disorders are also congenital” BUT lots of congenital disorders are not genetic (e.g. abnormalities because the mother was infected by CMV during pregnancy, not genetic)

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7
Q

Identify the main congenital and genetic renal diseases.

A

1) Renal hypoplasia
-Congenital
-One small kidney or no kidney, and other one is slightly larger
-If hypoplasia happens with renal artery stenosis, the small bit of kidney will produce more renin (because not getting enough oxygen) so paradoxically, stays protected but the rest of the body becomes subject to
hypertension because of renin production.
-Renal hypoplasia is also associated with Vesicoureteric reflux “retrograde regurgitation of urine from the urinary bladder up the ureter and into the collecting system of the kidneys”

2) Potter’s Syndrome (bilateral renal agenesis)
- Congenital
- No kidneys form
- No amniotic fluid
- Classically, child growing has flattened features because nothing cushioning it
- Often fatal in utero or immediately after birth

3) Polycystic Kidney Disease
- Genetic disease, may or MAY NOT be congenital
- Patients who present as children, and those that present as adults, present differently
- In children: Autosomal recessive. Tends to be more severe (present with renal failure) and happens sooner
- In adults: Autosomal dominant. More common. Present later. Present with mass, pain, possible sudden onset pain due to potential bleeds, urine leaks, possible reduced oxygenation of kidney leading to renin production and high BP. Loss of nephrons leading to excretory failure.
- Polycystic Kidney Disease significant because tends to lead to renal failure and therefore accounts for some patients on dialysis

Also: Familial Mediterranean Fever, Alport’s Syndrome (both genetic)

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8
Q

Identify the main types of Glomerular Disease.

A

• Primary
– Glomerulonephritis

• Secondary
– Vascular (hypertension), autoimmune (e.g. SLE, amyloid, diabetes, acquired)

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9
Q

Define glomerulonephritis.

A

Set of diseases with an immunological basis involving inflammation of the glomerulus and nephron (have been described associations with MHC/HLA antigens)).

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10
Q

Identify the types of Hypersensitivities associated with glomerulonephritis.

A

Type I- Immediate, IgE mediated NOT ASSOCIATED WITH GN

Type II- Antibody dependent (complement mediated cytolysis), with antibody targeted to part of the glomerulus

Type III- Immune Complexes (circulating antigens form immune complexes. Instead of being removed as normal, they persist (e.g. because too small) then stay in
circulation, and eventually may get stuck in a glomerulus)
Type IV- Cell mediated immunity (T cell, cytokines)

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11
Q

Describe the pathogenesis, and time frame of GN caused by type II hypersensitivity.

A

RAPIDLY PROGRESSIVE GN (AKA CRESCENTIC GN)

  • Entire glomerulus is affected
  • Antibodies formed against glomerular BM (may also cross react with alveolar BM in lungs)
  • Complement fixation occurs, membrane attack complex forms
  • All this results in damage including focal disruption of BM, and focal loss of podocytes
  • This allows plasma constituents into the Bowman space, including coagulation factors (which are proteins) and inflammatory mediators.
  • Fibrin forms, and there is proliferation of parietal epithelial cells and influx of macrophages, resulting in crescent formation (crescents = proliferation of parietal epithelium and inflammatory cells).
  • Eventually, this proliferation may compress capillaries, resulting in disruption of blood supply to nephrons, which then die (permanent)

Time frame is acute, process can happen in a week.

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12
Q

Describe the clinical presentation, and treatment of rapidly progressive GN.

A

CLINICAL PRESENTATION

  • Acute (occurs fast)
  • May be polyuric initially (due to ischemic tubules), but then decreased urine (eventually no kidney function so requires dialysis and transplant)
  • While still producing urine, haematuria, possibly some proteinuria
  • Lung involvement
  • Loin pain (because kidney stretched so stretches its capsule)

TREATMENT: Filter out antibody from plasma

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13
Q

What are the commonest causes of rapidly progressive GN ?

A
  • Goodpasture– autoimmune (most common cause)
  • Vasculitis- ANCA
  • SLE
  • Organic solvents
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14
Q

Identify the main kinds of GN caused by type III hypersensitivity.

A

Proliferative GN

Membraneous GN

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15
Q

Describe the pathogenesis, and time frame of proliferative GN.

A

PROLIFERATIVE GN (because mesengial cells proliferate)

  • Accumulation of numerous subepithelial immune complexes
  • Less prominent subendothelial immune complexes (size of IC determines where deposition occurs) are associated with endothelial cell proliferation and are related to increased capillary permeability and narrowing of the lumen
  • Frequently, proliferation of mesangial cells and a thickened mesangial matrix (BM) result in widening of the stalk and conspicuous trapping of immune complexes.
  • May or may not get complement fixation

TIME FRAME:
More gradual than rapidly progressive, but still relatively fast and acute

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16
Q

Describe the clinical presentation, and treatment of proliferative GN.

A

-Not as severe as rapidly progressive GN
-More gradual than rapidly progressive GN, but still relatively acute and fast
-May be either increased or decreased urine production
(at severe end, acute renal failure)
-Some haematuria but less than in rapidly progressive GN (focal damage as immune complex goes through BM, but not happening all the time)
-Some proteinuria but small amount, only reflecting amount of inflammation in glomerulus
-Loin pain (kidney stretched so stretches its capsule)

All these signs and symptoms add up to NEPHRITIC SYNDROME.

TREATMENT: Deal with infection (because cause often infectious)

17
Q

Identify the main causes of proliferative GN.

A
  • Post-infectious–Strep (immune complexes related to strep) (should be reversible, natural course is resolution as long as infection is addressed, since at that point immune complexes stop being formed)
  • Vasculitis- ANCA (Anti-Neutrophilic Cytoplasmic Autoantibody)
  • SLE
18
Q

Describe the pathogenesis, and time frame of membraneous GN.

A

MEMBRANEOUS GN
-Subepithelial accumulation of immune complexes (smaller ICs) and accompanying changes in the basement membrane (BM).
-Initially, scattered subepithelial deposits. The outer contour of the basement membrane remains smooth.
-Then, newly formed basement membrane has surrounded the deposits.
-Eventually, the immune complex deposits lose their electron density, resulting in an irregularly thickened basement membrane.
-Entire glomerulus ganged up with immune complexes so
glomerulus leaks
-Not very inflammatory

TIME FRAME: Indolent

19
Q

Describe the clinical presentation of membraneous GN.

A

-Indolent presentation
-No haematuria, severe proteinuria
-Edematous (because albumin leaks through, no osmotic P)
-Hyperlipidemia
(Affects males more than females and mainly adults)

These signs and symptoms add up to NEPHROTIC SYNDROME

20
Q

Identify the main causes of membraneous GN.

A
  • 15% over 70y patients with membraneous GN have cancer (ICs likely related to cancer) (hence to treat this for these patients, get rid of tumor)
  • Hepatitis B
  • Idiopathic
  • Penicillamine
  • SLE
21
Q

Define mesangiocapillary GN.

A

Both mesengial and capillary damage.

22
Q

Identify the main types of GN.

A 
Rapidly Progressive (type II)
Proliferative (type III)
Membraneous (type III)
Mesangiocapillary
Minimal Lesion (type IV) (and Focal and segmental glomerulosclerosis)
Focal and Segmental Necrotising GN
23
Q

Describe the pathogenesis of GN associated with type IV hypersensitivity.

A

MINIMAL LESION GN

  • Predominantly epithelial cell changes, particularly effacement of foot processes. All other glomerular structures appear intact.
  • Probably due to T cell mediated response
24
Q

Describe the clinical presentation, and treatment of minimal lesion GN.

A
  • Especially in children
  • Marked proteinuria (nephrotic)
  • Occasional association with Hodgkin’s Lymphoma
  • Measles seems to cause remission

TREATMENT:
Steroids

25
Q

Identify a possible complication of minimal lesion GN.

A

Some minimal lesions GN patients that don’t recover get focal scarring within glomerulus (Focal and segmental glomerulosclerosis).
Associated with proteinuria but no IC.

26
Q

What are the main GNs which lead to nephrotic syndrome ?

A

Minimal lesion
FSGS
Membranous

27
Q

What are the main components of nephrotic syndrome ? Explain why these components come about.

A
  • Proteinuria
  • Hyperlipidemia
  • Edema
  • Hypoproteinemia (including hypoalbuminemia)

Glomerular damage (from minimal lesion GN, FSGS, or membraneous GN) leads to increased permeability of glomerular capillaries to proteins, which leads to proteinuria. This leads to hypoproteinemia.

This in turn leads to decreased plasma oncotic P so fluid escapes into tissues leading to edema.
In the meantime, decreased plasma oncotic P also leads to decreased plasma V, thus decreased GFR, thus increased aldosterone secretion, thus fluid retention, thus edema.

Hypoproteinemia also leads to compensatory synthesis of proteins (including lipoproteins) by the liver, which leads to hyperlipidemia.

28
Q

What are the main GNs which lead to nephritic syndrome ?

A

Proliferative GN

Mesangiocapillary GN

29
Q

What are the main components of nephritic syndrome ? Explain why these components come about.

A

Proteinuria (less than in nephrotic syndrome)
Haematuria
Oligouria
Pain

30
Q

Identify causes of proteinuria other than GN.

A

• Diabetes: Glucose molecules onto proteins in BM, BM loses its electrical charge, and so proteins get in
but cannot get through, so clogs the filter (so begins to leak)
• Amyloidosis

31
Q

Identify vascular causes of glomerular disease.

A
  • Hypertension
  • Vasculitis
  • Mesangial IgA disease (IgA deposition, proliferative patterns with mesengial response. Indolent. Present with hypertension or hematuria. Significant cause of renal failure)
  • TTP
  • HUS
32
Q

Describe the pathophysiology and time frame of Focal and segmental necrotising GN.

A

Focal and Segmental Necrotising GN

  • Similar to FSNG but acute
  • Instead of scarring, necrosis of parts
  • Holes, fibrin leaking through into Bowman space (can get crescents)
33
Q

What are the main causes of Focal and segmental necrotising GN ?

A

Focal and segmental necrotising GN typically occurs in vasculitis or SLE.

34
Q

What are the main classes of diseases which affect the kidney ?

A
  • Glomerular disease

- Tubulointerstitial disease

35
Q

Identify the main kinds/causes of Tubulointerstitial disease.

A
  • Interstitial nephritis
  • Drug hypersensitivity
  • Acute tubular necrosis
  • Shock
  • Ascending infection (resulting in pyelonephritis, huge scarring and abscess formation))
  • SLE
  • Ischaemia
36
Q

Describe the main features of acute tubular necrosis.

A

Sloughing and necrosis of epithelial cells result in cast formation. Casts lead to obstruction and increased intraluminal pressure, which reduces glomerular filtration.

37
Q

Describe interstitial nephritis.

A

Inflammation of the interstitial tissue of the kidney, including the tubules.

MD3002 (95 decks)

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