Renal Disease Flashcards

(55 cards)

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
Proximal tubular dysfunction characterized by Impaired ability to REABSORB SODIUM
Bartter’s Syndrome
26
Proximal tubular dysfunction characterized by Impaired ability to REABSORB BICARBONATE
Renal Tubular Acidosis Type II
27
Proximal tubular dysfunction characterized by Impaired ability to REABSORB CALCIUM
Idiopathic Hypercalciuria
28
Proximal tubular dysfunction characterized by Excessive REABSORPTION of CALCIUM
Hypocalciuric Familial Hypercalcemia
29
Proximal tubular dysfunction characterized by Excessive REABSORPTION of SODIUM
Gordon’s Syndrome
30
Proximal tubular dysfunction characterized by Excessive REABSORPTION of PHOSPHATE
Pseudohypo parathyroidism
31
Generalized LOSS OF PROXIMAL TUBULAR FUNCTION
Fanconi Syndrome
32
These substances are NOT REABSORBED from the ULTRAFILTRATE & EXCRETED in the URINE in cases of Fanconi Syndrome
AA, Glucose, Water, Phosphorous, Potassium, & Calcium
33
Distal Tubular Dysfunction characterized by Impaired ability to REABSORB PHOSPHATE
Familial Hypophosphatemia (Vitamin D Resistant Rickets)
34
Distal Tubular Dysfunction characterized by Impaired ability to REABSORB CALCIUM
Idiopathic Hypercalciuria
35
Distal Tubular Dysfunction characterized by Impaired ability to ACIDIFY URINE
Renal Tubular Acidosis, Types I and IV
36
Distal Tubular Dysfunction characterized by Impaired ability to RETAIN SODIUM
Renal Salt-Losing Disorder
37
Distal Tubular Dysfunction characterized by Impaired ability to CONCENTRATE URINE
Nephrogenic Diabetes
38
Distal Tubular Dysfunction characterized by Excessive reabsorption of SODIUM
Liddle’s Syndrome
39
Distal Tubular Dysfunction characterized by Inability to REABSORB INORGANIC PHOSPHATES
Renal Phosphaturia
40
Types of Lower UTI
Urethritis (urethra) and Cystitis (Bladder)
41
Symptoms in Lower UTI
Painful urination Burning sensation Frequent urge to urinate
42
Types of Upper UTI
- Renal Pelvis Alone (Pyelitis) - Renal Pelvis including Interstitium (Pyelonephritis)
43
Bacterial infection that involves the renal tubules, interstitium, & renal pelvis
Acute Pyelonephritis
44
Mechanisms in Acute Pyelonephritis
- Movement of bacteria from the lower urinary tract to the kidney - Localization of the bacteria from the bloodstream in the kidneys (hematogenous infection)
45
Develops when permanent inflammation of renal tissue causes permanent scarring that involves the renal calyces and pelvis
Chronic Pyelonephritis
46
Allergic response to the interstitium of the kidney
Acute Interstitial Nephritis
47
Most common cause of Acute Interstitial Nephritis
Acute Allograft Rejection of a transplanted kidney
48
Clinically change in Acute Renal Failure
- Decreased GFR - Azotemia - Oliguria (Urine output: <400MI)
49
In acute renal failure, this result from DECREASE renal blood flow (25% of cases) *give the mechanism
Pre-Renal [URINE SODIUM CONCENTRATION IS LOW – INCREASED AMOUNT OF SODIUM BEING REABSORBED]
50
In acute renal failure, renal damage that can result from glomerular, tubular or vascular disease process (Approx. 65% cases) *give the mechanism
Renal [INCRASED URINARY EXCRETION OF SODIUM]
51
The mechanism in acute renal failure that result to obstruction of urine flow (Approx. 10% cases)
Post Renal
52
Progressive LOSS of RENAL FUNCTION caused by: IRREVERSIBLE & INTRINSIC RENAL DISEASE
Chronic Renal Failure
53
What happens to the GFR in Chronic Renal Failure?
Decreasing slowly but continuously
54
Chronic Renal Failure that progresses to advanced renal disease
END-STAGE RENAL DISEASE” / “END-STAGE KIDNEYS
55
Give the percentage of Calculi/stones
Calcium - 75% (Oxalate: 35%; Phosphate: 15%; Others: 25%) Magnesium Ammonium Phosphate - 15% Uric acid - 6% Cystine - 2%