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AUBF Renal and Metabolic Dse. > Renal Disease > Flashcards

Renal Disease Flashcards

1
Q

Most often are IMMUNE-MEDIATED

A

Glomerular

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2
Q

Result from INFECTIOUS or TOXIC SUBSTANCES

A

Tubular and Interstitial

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3
Q

Causes a renal perfusion that subsequently induces both MORPHOLOGIC & FUNCTIONAL changes in the kidney

A

Vascular

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4
Q

Glomerular Disease characterized by INCREASED permeability of the GLOMERULI to the passage of plasma proteins (ALBUMIN)

A

Nephrotic Syndrome

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5
Q

Amount of protein in Heavy Proteinuria

A

3.5g/day

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6
Q

Plasma albumin usually <3g/dL → LIVER SYNTHESIS unable to compensate for the large amount of protein EXCRETED in the urine

A

Hypoproteinemia

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7
Q

INCREASED plasma levels of TRIGLYCERIDES, CHOLESTEROL, PHOSPHOLIPIDS & VLDL

A

Hyperlipidemia

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8
Q

Caused by Post-Streptococcal Infection → known as: ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
(Blood: Elevated ASO titer)

A

Acute Glomerulonephritis

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9
Q

Causative agent of Acute glomerulonephritis and the protein found that induces this type of nephritis

A

Group A Beta-hemolytic Streptococci / M protein
Non-streptococcal (bacteria: pneumococci; virus: mumps and Hepa B; parasitic infection: Malaria)

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10
Q

SCLEROSIS of the GLOMERULI

A

Focal Segmental Glomerulonephritis

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11
Q

Predominant feature of Focal Segmental Glomerulonephritis

A

Proteinuria

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12
Q

Cellular Proliferation of the MESANGIUM along with LEUKOCYTE INFILTRATION & THICKENING OF THE GLOMERULAR BASEMENT MEMBRANE

A

Membranoproliferative Glomerulonephritis

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13
Q

Most prevalent type of glomerulonephritis world wide
Deposition of IgA in the GLOMERULAR MESANGIUM

A

IgA Nephropathy

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14
Q

Development: Slow and Silent
80%: have previously some form of glomerulonephritis
20%: form of glomerulonephritis that has been unrecognized

A

Chronic Glomerulonephritis

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15
Q

Destruction of RENAL TUBULAR Epithelial Cells

A

Acute Tubular Necrosis

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16
Q

Type of Acute Tubular Necrosis follows a HYPOTENSIVE event that result in decrease perfusion of the kidneys followed by renal tissue ischemia

A

ISCHEMIC ATN

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17
Q

Give the 3 Principal causes of Ischemic ATN

A

-Sepsis
-Shock
-Trauma

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18
Q

Type of Acute Tubular Necrosis results from exposure to NEPHROTOXIC AGENTS

A

TOXIC ATN

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19
Q

Normal solutes or substances that become toxic when their concentration in the bloodstream is excessive

A

Endogenous Nephrotoxin

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20
Q

Examples of Endogenous Nephrotoxin

A

Hemoglobin, Myoglobin, Uric acid, Immunoglobulin light chain

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21
Q

Nephrotoxin that are substances ingested or absorbed

A

Exogenous Nephrotoxin

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22
Q

Examples of Exogenous Nephrotoxin

A

Therapeutic agents, anesthetics, Radiographic contrast media, Chemotherapeutic drugs, Recreation drugs, Industrial chemicals

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23
Q

Proximal tubular dysfunction characterized by Impaired ability to REABSORBED GLUCOSE

A

Renal Glucosuria

24
Q

Proximal tubular dysfunction characterized by Impaired ability to REABSORBED SPECIFIC AMINO ACIDS

A

Cystinuria (Cystine and Dibasic AA) and Hartnup Disease (Monoamino – Monocarboxylic AA)

25
Q

Proximal tubular dysfunction characterized by Impaired ability to REABSORB SODIUM

A

Bartter’s Syndrome

26
Q

Proximal tubular dysfunction characterized by Impaired ability to REABSORB BICARBONATE

A

Renal Tubular Acidosis Type II

27
Q

Proximal tubular dysfunction characterized by Impaired ability to REABSORB CALCIUM

A

Idiopathic Hypercalciuria

28
Q

Proximal tubular dysfunction characterized by Excessive REABSORPTION of CALCIUM

A

Hypocalciuric Familial Hypercalcemia

29
Q

Proximal tubular dysfunction characterized by Excessive REABSORPTION of SODIUM

A

Gordon’s Syndrome

30
Q

Proximal tubular dysfunction characterized by Excessive REABSORPTION of PHOSPHATE

A

Pseudohypo parathyroidism

31
Q

Generalized LOSS OF PROXIMAL TUBULAR FUNCTION

A

Fanconi Syndrome

32
Q

These substances are NOT REABSORBED from the ULTRAFILTRATE & EXCRETED in the URINE in cases of Fanconi Syndrome

A

AA, Glucose, Water, Phosphorous, Potassium, & Calcium

33
Q

Distal Tubular Dysfunction characterized by Impaired ability to REABSORB PHOSPHATE

A

Familial Hypophosphatemia
(Vitamin D Resistant Rickets)

34
Q

Distal Tubular Dysfunction characterized by Impaired ability to REABSORB CALCIUM

A

Idiopathic Hypercalciuria

35
Q

Distal Tubular Dysfunction characterized by Impaired ability to ACIDIFY URINE

A

Renal Tubular Acidosis, Types I and IV

36
Q

Distal Tubular Dysfunction characterized by Impaired ability to RETAIN SODIUM

A

Renal Salt-Losing Disorder

37
Q

Distal Tubular Dysfunction characterized by Impaired ability to CONCENTRATE URINE

A

Nephrogenic Diabetes

38
Q

Distal Tubular Dysfunction characterized by Excessive reabsorption of SODIUM

A

Liddle’s Syndrome

39
Q

Distal Tubular Dysfunction characterized by Inability to REABSORB INORGANIC PHOSPHATES

A

Renal Phosphaturia

40
Q

Types of Lower UTI

A

Urethritis (urethra) and Cystitis (Bladder)

41
Q

Symptoms in Lower UTI

A

Painful urination
Burning sensation
Frequent urge to urinate

42
Q

Types of Upper UTI

A
  • Renal Pelvis Alone (Pyelitis)
  • Renal Pelvis including Interstitium (Pyelonephritis)
43
Q

Bacterial infection that involves the renal tubules, interstitium, & renal pelvis

A

Acute Pyelonephritis

44
Q

Mechanisms in Acute Pyelonephritis

A
  • Movement of bacteria from the lower urinary tract to the kidney
  • Localization of the bacteria from the bloodstream in the kidneys (hematogenous infection)
45
Q

Develops when permanent inflammation of renal tissue causes permanent scarring that involves the renal calyces and pelvis

A

Chronic Pyelonephritis

46
Q

Allergic response to the interstitium of the kidney

A

Acute Interstitial Nephritis

47
Q

Most common cause of Acute Interstitial Nephritis

A

Acute Allograft Rejection of a transplanted kidney

48
Q

Clinically change in Acute Renal Failure

A
  • Decreased GFR
  • Azotemia
  • Oliguria (Urine output: <400MI)
49
Q

In acute renal failure, this result from DECREASE renal blood flow (25% of cases) *give the mechanism

A

Pre-Renal [URINE SODIUM CONCENTRATION IS LOW – INCREASED AMOUNT OF SODIUM BEING REABSORBED]

50
Q

In acute renal failure, renal damage that can result from glomerular, tubular or vascular disease process (Approx. 65% cases) *give the mechanism

A

Renal [INCRASED URINARY EXCRETION OF SODIUM]

51
Q

The mechanism in acute renal failure that result to obstruction of urine flow (Approx. 10% cases)

A

Post Renal

52
Q

Progressive LOSS of RENAL FUNCTION caused by: IRREVERSIBLE & INTRINSIC RENAL DISEASE

A

Chronic Renal Failure

53
Q

What happens to the GFR in Chronic Renal Failure?

A

Decreasing slowly but continuously

54
Q

Chronic Renal Failure that progresses to advanced renal disease

A

END-STAGE RENAL DISEASE” / “END-STAGE KIDNEYS

55
Q

Give the percentage of Calculi/stones

A

Calcium - 75% (Oxalate: 35%; Phosphate: 15%; Others: 25%)
Magnesium Ammonium Phosphate - 15%
Uric acid - 6%
Cystine - 2%

AUBF Renal and Metabolic Dse. (2 decks)

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