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Mechanisms of Disease > Renal and Urinary Tract Diseases > Flashcards

Renal and Urinary Tract Diseases Flashcards

1
Q

Narrowing of at least one artery that supplies the kidney is known as?

A

Renal artery stenosis

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2
Q

In renal artery stenosis, what happens after blood flow and pressure into the kidneys get reduced?

A

Activates the renin-angiotensin system, BUT cannot raise pressure within the kidney due to the stenosis

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3
Q

What is the function of Juxtaglomerular (JG) cells?

A
  • Produce renin when arteriole pressure decreases
  • Increases blood pressure
  • Rate-limiting step for renin-angiotensin system
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4
Q

What is the function of the macula densa?

A

When arteriole pressure increases, there is less Na+ and Cl- reabsorption. This causes release vasoactive compounds to constrict arterioles and decrease GFR

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5
Q

What are the consequences of elevated arteriole pressure? (4)

A
  1. Increased pressure
  2. Increased fluid secretion
  3. Increased GFR
  4. Decreased reabsorption
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6
Q

What is the function of ACE? Where is it expressed?

A
  • Angiotensin-converting enzyme
  • Converts angiotensin → angiotensin II (AngII)
  • ~70-80% in lungs, 20% in kidneys
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7
Q

What is the function of AngII? (3)

A
  1. Potent vasoconstrictor that directly increases blood pressure
  2. Stimulates adrenal glands to release aldosterone
  3. Increased blood pressure shuts off renin release
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8
Q

What is the function of aldosterone in the renin-angiotensin system?

A
  1. Promote Na+ and water absorption in the kidney
  2. Increases blood volume, thereby increasing blood pressure
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9
Q

What are the consequences of renal artery stenosis?

A
  1. Reduced blood flow and pressure into the kidney
  2. High blood pressure (renal HTN)
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10
Q

What are the treatment options for renal artery stenosis? (2)

A

Administration of ACE inhibitors and/or stent placement

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11
Q

What is nephrosclerosis?

A
  • Sclerosis of arterioles and small arteries within the kidneys
  • Caused by, and a cause of, hypertension
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12
Q

What glomerular changes occur in nephrosclerosis? (3)

A
  1. Glomerular basement membrane (GBM) damage
  2. Collagen in in Bowman’s space
  3. Fibrosis around capsule
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13
Q

Nephrosclerosis can lead to _____ of the walls of blood vessels in the kidney

A

Hyalinization

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14
Q

Malignant HTN is a frequent cause of ____ in patients with systemic sclerosis

A

Renal failure

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15
Q

What are the symptoms of nephrosclerosis?

A
  1. Unresolved (malignant) HTN
  2. In diabetics, increased risk of renal failure
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16
Q

What type of endothelial damage occurs in nephrosclerosis? What are it’s consequences?

A
  1. Fibrinoid necrosis
  2. Hyperplastic arteriolitis
  • Results in protein leakage and development of clots; renal ischemia
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17
Q

Glomerular damage can be secondary to what other diseases? (4)

A
  1. Lupus
  2. Diabetes Mellitus
  3. Amyloidosis
  4. Goodpasture Syndrome
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18
Q

Primary glomerular diseases are typically ______

A

Autoimmune

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19
Q

What are the autoimmune causes of glomerular damage? (2)

A
  1. Circulating antigen:antibody complexes deposit in filtaration membrane
  2. Antibodies reacting against components of the filtration membrane
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20
Q

Nephritic syndrome refers to?

A
  • Glomerular inflammation
  • Proliferative changes and leukocyte infiltration
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21
Q

Nephrotic syndrome refers to?

A
  • Podocyte injury
  • Structural and /or phsyiolochemical alterations
  • Damage to glomerular membrane results in protein leakage
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22
Q

How does nephritic syndrome present clinically?

A
  1. Hematuria
  2. Oliguira with azotemia
  3. Proteinuria
  4. Hypertension
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23
Q

What is oliguria?

A

Significantly decreased urine production

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24
Q

What is azotemia?

A

Increased nitrogen containing compounds in the blood (BUN)

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25
Q

What are the most common causes of nephritic syndrome?

A
  1. Acute postinfectious glomerulonephritis
  2. Rapidly progressive glomerular nephritis (RPGN)
  • Immunologically-mediated
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26
Q

Describe the cascade of events that occurs in nephrotic syndrome following damage to the glomerular capillary walls.

A

Massive proteinuria → depletes serum albumin → hypoalbuminemia → reduces osmotic pressure → generalized edema → compensatory aldosterone secretion → hyperlipidemia and lipiduria

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27
Q

What is membranous nephropathy? Cause?

A
  • Diffuse thickening of capillary walls
  • Caused by Ig deposits or self-antibodies
28
Q

What is post-streptococcal glomerulonephritis?

A
  • Acute proliferative glomerulonephritis
  • Antibodies to streptococcal proteins will recognize glomerular proteins
  • Causes nephritic syndrome
29
Q

Goodpasture syndrome is described as?

A

Renal failure with pulmonary hemorrhage

30
Q

What is the cause of Goodpasture syndrome?

A
  • Anti-GBM in kidney (severe glomerular injury)
  • Anti-GBM recognizes collagen IV in alveolar basement membrane
31
Q

How does Goodpasture syndrome present clinically?

A
  1. Hemoptysis
  2. Hematuria
  3. Nephritic syndrome
  4. Potential nephrotic syndrome
32
Q

What are the treatment options for Goodpasture syndrome? (2)

A
  1. Plasmapheresis to remove antibodies
  2. Immunosuppression
33
Q

What is Crescentic Glomerulonephritis?

A
  • Rapid loss of renal function (RPGN)
  • Parietal cells fill urinary space
34
Q

What is acute pyelonephritis?

A
  • Tubulointerstitial nephritis
  • Bacterial infection due to UTI
  • Inflammation of interstitium and tubules
35
Q

What drugs can induce tubulointerstitial nephritis?

A
  1. Penicillin and other antibiotics
  2. NSAIDS
36
Q

If water ingestion exceeds urine excretion rate of _____ it leads to water intoxication

A

16 mL/min

37
Q

What is the major symptom of water intoxication?

A

Swelling of CNS neurons, which leads to:

  • Convulsions
  • Coma
  • Death
38
Q

Acute kidney injury (AKI) is the most common cause of?

A

Acute renal failure

39
Q

Acute renal failure is described as:

A
  • Rapid reduction of renal function
  • Urine output <400 mL/day (oliguiria to anuria)
40
Q

How much urine do the kidneys normally produce per day?

A

1.5 L/day

41
Q

50% of acute renal failure occurs _____

A

in patients hospitalized for other reasons

42
Q

What are the potential causes of AKI?

A
  1. Ischemia
  2. Directy toxic injury
  3. Inflammation
  4. Urinary obstruction
43
Q

How can AKI be treated?

A
  1. Prevention of further damage (address primary cause)
  2. Antibiotics to prevent secondary infection
  3. Diuretics to flush out the kidneys
  4. Dialysis
44
Q

In AKI, is necrosis more typically found in the proximal or distal tubules?

A

Proximal tubules

45
Q

Chronic kidney disease (CKD) is described as:

A
  • Significantly decreased GFR and/or albuminuria for 3 months
  • Irreversible loss of tubular cells
46
Q

True or false. AKI can resolve through regeneration

A

True

47
Q

What are some causes of chronic kidney disease (3)? Most chronic (***)?

A
  1. ***Diabetes mellitus
  2. Hypertension
  3. Glomerulonephritis
48
Q

What are the treatment options for chronic kidney disease? (4)

A
  1. Treat underlying cause (HTN, diabetes, etc)
  2. Change in diet and lifestyle
  3. Dialysis
  4. Transplant
49
Q

In general, altered kidney function affects (4):

A
  1. Sodium and potassium homeostasis
  2. Water balance
  3. Acid-base balance
  4. Urea excretion
50
Q

Excess sodium expands intravascular volume, which increase reabsorption. This can lead to (2):

A
  1. Hypertension
  2. Congestive heart failure
51
Q

Accumulation of nitrogenous waste products due to kidney failure is known as?

A

Uremia

52
Q

What are the symptoms of Uremia? (4)

A
  1. Decreased appetite
  2. Fatigue
  3. Neurological symptoms (confusion or coma)
  4. Skin excretion (uremic frost)
53
Q

Uremia can result from (3):

A
  1. Hypotension
  2. Dehydration
  3. Trauma (increased protein catabolism)
54
Q

Why can CKD result in low calcium?

A

Kidneys are no longer able to activate vitamin D, which is essential for calcium and phosphate absorption

55
Q

What is renal osteodystrophy?

A
  • Lack of vitamin D reduces intestinal Ca2+ absorption
  • Parathyroid hormone (PTH) increases osteoclast activity
56
Q

What is the most common site for kidney stones?

A

Renal pelvis and calyces

57
Q

What are some causes of kidney stones?

A
  1. Genetics
  2. Dehydration
  3. Dietary intake
  4. Hormonal imbalance (parathyroid tumor)
58
Q

75% of kidney stones are composed of

A

Calcium oxalate and/or calcium phosphate

59
Q

Besides calcium, what are some other types of kidney stones?

A
  1. Uric acid (<10%)
  2. Cystine (1%)
  3. Infection (15%)
60
Q

What is hydronephrosis?

A

Expansion of the renal pelvis anc calyces due to obstruction downstream

61
Q

How can kidney stones be treated?

A
  1. Pain management
  2. Prevent dehydration
  3. Shock waves (lithotripsy)
  4. Stent placement
  5. Prevent new stones (allopurinol inhibits purine catabolism to decrease uric acid)
  6. “Rollercoasters”
62
Q

What is the main difference between acute and chronic cystitis?

A
  • Acute: neutrophil infiltrates
  • Chonric: mononuclear infiltrate (macrophages & T-cells)
63
Q

What is cystitis?

A

Bladder inflammation

64
Q

What are the different types of cystitis? (5)

A
  1. Bacterial
  2. Hemorrhagic
  3. Interstitial (b/w cells)
  4. Malakoplakia (defect in phagocytic cells)
  5. Polypoid
65
Q

What are the most common species that cause cystitis (4)? Most common (***)?

A
  1. ***E. coli
  2. Proteus
  3. Klebsiella
  4. Enterobacter
66
Q

What is the “symptom triad” of cystitis?

A
  1. Frequency (up to every 15-20 minutes)
  2. Lower abdominal pain
  3. Dysuria

Mechanisms of Disease (13 decks)

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