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Renal Module > Renal Path > Flashcards

Renal Path Flashcards

1
Q

What is Azotemia?

A

Azotemia is a biochemical abnormality that refers to an elevation of the blood urea nitrogen and creatinine levels, and is largely related to decreased GFR. A consequence of many renal disorders.

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2
Q

When is prerenal azotemia encountered?

A

When there is hypoperfusion of the kidneys (e.g in hemorrage, shock, volume depletion and CHF) that impairs renal function in the absence of parenchymal damage.

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3
Q

When is postrenal Azotemia seen?

A

Whenever urine flow is obstructed beyond the level of the kidney.

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4
Q

What is Nephritic syndrome?

A

Is due to glomerular disease and is dominated by the acute onset of usually grossly visible hematuria, mild to moderate proteinuria, and hypertension; it is the classic presentation of acute poststreptococcal glomerulonephritis.

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5
Q

What is rapidly progressive glomerulonepritis?

A

Characterized as a nephritic syndrome with rapid decline in GFR (hours to days)

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6
Q

How long does the decline of GFR take in rapidly progressive glomerulonepritis?

A

Hours to days.

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7
Q

What is Nephrotic Syndrome?

A

Due to glomerular disease and is characterized by heavy proteinuria (more than 3.5gm/day), hypoalbuminemia, severe edema, hyperlipidemia, and lipid in the urine (lipiduria)

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8
Q

What is Asymptomatic hematuria or proteinuria?

A

One or a combination of these two is usually a manifestation of subtle or mild glomerular abnormalities

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9
Q

What is acute renal failure?

A

Dominated by oliguria or anuria, and recent onset of azotemia. It can result from glomerular, interstitial, or vascular injury

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10
Q

What is Chronic Kidney failure?

A

Characterized by prolonged symptoms and signs of uremia, is the end result of all chronic renal parenchymal diseases

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11
Q

What are the chief signs of Renal tubular defects?

A

1.Polyuria
2.Nocturia
3.Electrolyte disorders (e.g metabolic
acidosis)

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12
Q

What are the main causes of renal tubular diseases?

A

1.Diseases that directly affect the tubular
structure
2.Diseases that cause defects in specific
tubular functions which could be either
inherited (familial nephrogenic diabetes,
cystinuria, renal tubular acidosis) or
acquired (e.g lead neuropathy)`

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13
Q

What characterizes UTI?

A

Bacteriuria and pyuria (bacteria and leukocytes in the urine).

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14
Q

What is Pyelonephritis?

A

Kidney infection (pyelonephritis) is a specific type of urinary tract infection (UTI) that generally begins in your urethra or bladder and travels up into your kidneys.

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15
Q

What is Cystitis?

A

Cystitis is the medical term for inflammation of the bladder. Most of the time, the inflammation is caused by a bacterial infection, and it’s called a urinary tract infection (UTI). A bladder infection can be painful and annoying, and it can become a serious health problem if the infection spreads to your kidneys.

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16
Q

What is Nephrolithiasis?

A

Manifested by severe spasms of pain (renal colic) and hematuria often with frequent stone formation.

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17
Q

What is the major cause of death in most Renal disease?

A

Chronic renal failure

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18
Q

How many stages of renal failure are there?

A

4

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19
Q

Describe Stage I or Diminished renal reserve

A

1.GFR is about 50% of normal

2.Serum BUN and Creatinine values are
normal and the patients are Asymptomatic

3.More susceptible to developing Azotemia.

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20
Q

Describe stage II renal failure (Renal insufficiency)

A
  1. The GFR is 25-50% of Normal
  2. Azotemia is present
  3. Usually associated with anemia and hypertension
  4. Polyuria and nocturia can occur as a result of decreased concentrating ability
  5. Sudden stress (nephrotoxins) may precipitate uremia
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21
Q

Describe Stage III renal failure (Chronic renal failure)

A
  1. GFR is less than 20-25% of normal
  2. Kidneys cannot regulate volume and solute composition so the patient develops edema, metabolic acidosis, and hyperkalemia.
  3. Overt uremia may ensue, with neurologic, GI, and cardiovascular complications.
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22
Q

Describe stage IV renal failure (End-Stage renal disease)

A
  1. GFR is less than 5% of normal

2. Terminal stage of Uremia

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23
Q

What is one of the most common causes of Chronic kidney disease?

A

Chronic Glomerulonephritis

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24
Q

What hereditary disease frequently affects the glomerulus?

A

Fabry disease

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25
What is Fabry disease?
is a rare X-linked (inherited) lysosomal storage disease, which can cause a wide range of systemic symptoms. It is a form of sphingolipidosis, as it involves dysfunctional metabolism of sphingolipids.
26
What are the principal manifestations of chronic kidney disease and uremia in Fluid and Electrolytes?
1. Dehydration 2. Edema 3. Hyperkalemia 4. Metabolic acidosis
27
What are the principal manifestations of chronic kidney disease and uremia in Calcium phosphate and bone?
1. Hyperphosphatemia 2. Hypocalcemia 3. Secondary hyperparathyroidism 4. Renal Osteodystrophy
28
What are the principal manifestations of chronic kidney disease and uremia in Hematologic system?
1. Anemia | 2. Bleeding Diathesis
29
What are the principal manifestations of chronic kidney disease and uremia in Cardiopulmonary system?
1. Hypertension 2. CHF 3. Cardiomyopathy 4. Pulmonary edema 5. Uremic Pericarditis
30
What are the principal manifestations of chronic kidney disease and uremia in GI system?
1. Nausea and vomitting 2. Bleeding 3. Esophagitis, gastritis, colitis
31
What are the principal manifestations of chronic kidney disease and uremia in Neuromuscular system?
1. Myopathy 2. Peripheral neuropathy 3. Encephalopathy
32
What are the principal manifestations of chronic kidney disease and uremia in Dermatologic system?
1. Swallow color 2. Pruritus 3. Dermatitis
33
What are the primary Glomerulopathies?
1. Acute proliferative glomerulonephritis - Post infectious - Other 2. Rapidly progressive (cresentic) glomerulonephritis 3. Membranous Glomerulopathy 4. Minimal-change disease 5. Focal segmental glomerulosclerosis 6. Membranoproliferative glomerulonephritis 7. IgA Nephropathy 8. Chronic Glomerulonephritis
34
What are the secondary / Systemic diseases with Glomerular involvement?
1. Systemic Lupus Erythmatosus 2. Diabetes Mellitus 3. Amyloidosis 4. Goodpasture syndrome 5. Microscopic polyarteritis/polyangiitis 6. Wegener Granulomatosis 7. Henoch-Shonlein Purpura 8. Bacterial endocarditis
35
What are the hereditary disorders with Glomerular involvement?
1. Alport Syndrome 2. Thin Basement Membrane disease 3. Fabry disease
36
What is the thick electron dense layer of the GBM know as?
Lamina Densa
37
What is the GBM mostly made of?
1. Type IV collagen 2. Laminin 3. Polyanionic proteoglycans (Mostly Heparan Sulfate) 4. Fibronectin 5. Entactin The Type IV collagen forms a network suprastructure to which other glycoproteins attach.
38
Which cells form the visceral epithelium of the Glomerulus?
The podocytes.
39
What are the Renal mesangial cells?
These cells are of mesenchymal origin, are contractile, phagocytic, and capable of proliferation, of laying down both matrix and collagen, and of secreting bilogically active mediators.
40
What are the (4) Basic tissue reactions in Glomerulopathies?
1. Hypercellularity 2. Babsement Membrane Thickening 3. Hyalinosis 4. Sclerosis
41
What is characterizes the hyperycellularity of Glomerulopathies?
Increase in the number of cells in the Glomerular tuft via 1. Cellular proliferation 2. Leukocytic infiltration (newutrphisl, monocytes and in some diseases lymphocytes) 3. Formation of Cresecents -These are accumulations of cells composed of proliferating parietal epithelial cells and infiltrating leukocytes.
42
How are Crescents formed?
Fibrin leaks in the urinary space often through ruptured basement membrane and elicits the crescentic response.
43
How does Basement membrane thickening appear on light microscopy?
Appears as thickening of the capillary walls best seen with Periodic Acid-Schiff stain.
44
How does basement membrane thickening appear on electron microscopy?
1. Deposition of amorphous electron dense material, most often immune complexes, on the endothelial or epithelial side of the basement membrane or within the GBM itself. 2. Thickening of the basement membrane due to increased synthesis of its protein components as occurs in diabetic glomerulosclerosis.
45
What is meant by Hyalinosis?
Hyalinosis as applied to the glomerulus denotes the accumulation of material that homogenous and eosinophilic by light microscopy. 2.By electron microscopy the hyalin is extracellular and amorphous. It is made up of plasma proteins that have insudated from the circulation in glomerular structures .
46
What is Hyalinosis usually the result of?
Hyalinosis is usually a result of endothelial and capillary wall injury, It is a common feature of Focal segmental Glomerulosclerosis.
47
What is sclerosis?
Characterized by accumulations of extracellular collagenous matrix, either confined to mesangial matrix areas as is the case in diabetic glomerularsclerosis, or involving the capillary loops or both.
48
What is the anti-gen responsible for classic anti-GBM antibody-induced glomerulonephritis and Goodpasture syndrome?
A component of the noncollagenous domain (NC1) of the ALPHA3 chain of type IV collagen.
49
How are most instances of anti-GBM antibody induced glomerulonephritis characterized?
By severe crescentic glomerular damage and the clinical syndrome of rapidly progressive glomerulonephritis.
50
What is Circulating Immune complex Glomerulonephritis?
In this type of nephritis glomerular injury is caused by the trapping of circulating antigen-antibody complexes within the Glomeruli.
51
Do the circulating immune complexes have specificity for glomerular components?
No. They localize in the Glomerulus because of their physiochemical properties.
52
What are some of the exogenous antigen that may trigger formation of complexes that subsequently cause glomerular damage?
1. Bacterial Products (Streptococci) 2. Surface antigen of Hep B 3. Hep C virus antigens 4. Antigen of - Treponema Pallidum ( syphilis etc) - Plasmodium Falciparum (Malaria)
53
What do the glomerular lesions usually exhibit in Circulating Immune complex Glomerulonephritis?
Leukocytic infiltration and proliferation of mesangial and endothelial cells.
54
What would the electron microscope scan show in Circulating Immune complex Glomerulonephritis?
It would reveal the immune complexes as electron-dense deposits that lie in the mesangium, between the endothelial cells and GBM (subendothelial deposits)
55
What would immnunofluorescence microscopy show in Circulating Immune complex Glomerulonephritis?`
Granular deposits along the basement membrane, in th mesangium or in both locations.
56
What factors play a role in glomerular localization of Antigen, antibody, or complexes or both?
1. The molecular charge | 2. The Molecular size
57
What do highly cationic immunogens do?
Ten to Cross the GBM, and the resultant complexes eventually reside in a subepithelial location.
58
What do highly anionic macromolecules do?
Highly anionic Macromolecules are excluded from the GBM and either are trapped subendothelially or are not nephritogenic at all.
59
What do neutral macromolecules do?
Tend to accumulate in the mesangium.
60
What tends to happen to large circulating complexes?
The are usually cleared by the mononuclear phagocyte system and do not enter the GBM in sufficient quantities
61
What type of deposits are in IGA nephropathy?
Mesangial deposits
62
What type of deposits are in Lupus nephritis and membranoproliferative glomerulonephritis?
Subendothelial
63
What is (FSGS) Focal segmental Glomerulosclerosis?
Patients with this secondary change develop proteinuria even if the primary disease is nonglomerular. The Glomerulosclerosis seems to be initiated by adaptive change in the relatively unaffected glomeruli of diseased kidneys. E.G compensatory hypertrophy.

Renal Module (29 decks)

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