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Mechanism of Disease > Exam 2: Renal and Urinary Tract Disease > Flashcards

Exam 2: Renal and Urinary Tract Disease Flashcards

1
Q

Overview

Kidney disease is classified by __

A

Cause

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2
Q

Causes of Kidney Disease

Pre-renal

A

Volume depletion (including sweat loss and hemorrhage)
Hypotension
Heart failure
stenosis
cirrhosis
NSAIDs

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3
Q

Causes of kidney disease

Intrarenal

A

Vascular (sclerosis, vasculitis)
Glomerular (membrane damage)
Tubular (cancer, toxic injury, altered ionic homeostasis

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4
Q

Causes of kidney disease

Postrenal

A

Obstruction
Stones
Prostatic disease

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5
Q

Pre-Renal Kidney Disease

Renal Artery Stenosis

A

Narrowing of at least one artery that supplies the kidneys

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6
Q

Pre-Renal Kidney Disease

What does Renal Artery Stenosis do to the kidneys?

A

Reduces blood flow and pressure into the kidneys
Activates renin-angiotensin system
cannot raise pressure within the kidney

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7
Q

Pre-Renal Kidney Disease

What causes the thickened tunica media in Renal Artery Stenosis?

A

Excess smooth muscle
fibrosis

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8
Q

Pre-Renal Kidney Disease

How is blood pressure regulated in the kidney?

A

Juxtaglomerular apparatus at vascular pole
Specialized JG cells produce renin
Macula densa cells detect ions

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9
Q

Pre-Renal Kidney Disease

What causes elevated arteriole pressure?

A

Higher glomerular filtration rate aters ionic concentration
Release of vasoactive compounds constricts arteriole, which decreases GFR
Lower NA+, Cl- concentration stops release

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10
Q

Pre-Renal Kidney Disease

How does a higher glomerular filtration rate alter ionic concentration in the kidney? How is it detected?

A

Less sodium and chloride can be recovered
Detected by cells in macula densa

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11
Q

Pre-Renal Kidney Disease

What does decreased arteriole pressure do in the kidneys?

A

Stimulates juxtaglomerular cells and release of renin

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12
Q

Pre-Renal Kidney Disease

Renin-Angiotensin System

A

JG cells release Renin from kidney
cleaves angiotensinogen into angiotensin I
Angiotensin-converting enzyme converts angiotensin I to angiotensin II
Angiotensin II causes vasoconstriction (decreased vascular space) in cardiovascular system and salt/water retention in kidneys (increases blood volume) - together increase BP

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13
Q

Pre-Renal Kidney Disease

What is the rate limiting step in the Renin-Angiotensin system?

A

Serum renin concentrations
System is controlled by JG cells in kidneys

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14
Q

Pre-Renal Kidney Disease

Where is angiotensin converting enxyme (ACE) found? How much Angiotensin II is converted in the kidneys?

A

Lung capillaries (also kidneys and other organs) express the enzyme
20% is converted

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15
Q

Pre-Renal Kidney Disease

Angiotensin II

A

Potent vasoconstrictor that directly increases blood pressure

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16
Q

Pre-Renal Kidney Disease

How does angiotensin II increase blood pressure? What does it do?

A

Stimulates adrenal glands to release aldosterone - promotes Na+ and water absorption in kidneys - increases blood volume - increases BP - increases BP shuts off renin release

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17
Q

Pre-Renal Kidney Disease: Renal Artery Stenosis

What are the symptoms of Renal Artery Stenosis?

A

High Blood Pressure (Renal HTN) (hyper tension in kidney, hypotension outside kidney)
Symptoms of Kidney Injury

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18
Q

Pre-Renal Kidney Disease: Renal Artery Stenosis

What are the causes of Renal Artery Stenosis?

A

Most common: athersclerosis
Less common: fibromuscular dysplasia
Decrease lumen - stenosis

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19
Q

Pre-Renal Kidney Disease: Renal Artery Stenosis

What are the treatments for Renal Artery Stenosis?

A

ACE inhibitors
Stent in renal artery/vessel

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20
Q

Intrarenal: Nephrosclerosis

Nephrosclerosis

A

Sclerosis of arterioles and small arteries within the kidneys

AKA Patchy atrophic ischemia

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21
Q

Intrarenal: Nephrosclerosis

What is the cause of Nephrosclerosis? What does it cause?

A

Caused by, and cause of, hypertension
Hylainization of vessel walls
genetics, age, general HTN

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22
Q

Intrarenal: Nephrosclerosis

What are the glomerular changes in Nephrosclerosis?

A

Partial to total sclerosis
GBM damage, collagen in Bowman’s space
Fibrosis around capsule

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23
Q

Intrarenal: Nephrosclerosis

What are the tubular changes in Nephrosclerosis?

A

Loss of tubules

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24
Q

Intrarenal: Nephrosclerosis

What is the result of vessel wall hyalinization in Nephrosclerosis?

A

Fibrin leaks through endothelium into vessel walls
Form smooths appearing eosinophilic membrane

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25
Q

Intrarenal: Nephrosclerosis

What are the clinical symptoms of Nephrosclerosis?

A

Unresolved HTM, diabetes increase risk of renal failure

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26
Q

Intrarenal: Nephrosclerosis

Does nephrosclerosis present with symptoms of clinical renal failure?

A

If nephrosclerosis is the only disease present, rare to present with symptoms of clinical renal failure

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27
Q

Intrarenal: Nephrosclerosis

Malignant HTN (unresolved HTN)

A

Endothelial damage results in protein leakage and development of clots
leads to renal ischemia (fibrinoid necrosis, hyperplastic arteriolitis)

Also frequent cause of renal failure in patients with sytemic sclerosis

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28
Q

Intrarenal: Nephrosclerosis

What effect does involvement of afferent arterioles have on unresolved HTN?

A

Leads to renin elevation

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29
Q

Intrarenal: Glomerular Damage

What are the causes of Glomerular Damage?

A

Secondary effects of systemic diseases
Circulating antigen:antibody complexes deposit in filtration membrane
Antibodies reacting against components of the filtration membrane

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30
Q

Intrarenal: Glomerular Damage

Primary glomerular disease starts in the…

A

Kidney

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31
Q

Intrarenal: Glomerular Damage

Where do immune complexes deposit?

A
  1. Podocyte effacement (between podocyte and their BM)
  2. Subepithelial deposits (In BM, but exterior to Lamina densa under podocytes)
  3. Subendothelial deposits (between endothelial cells and lamina densa)
  4. Mesangial deposits (mesangial membrane)
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32
Q

Intrarenal: Glomerular Damage

What disease is podocte effacement associated with?

A

Minimal change disease

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33
Q

Intrarenal: Glomerular Damage

What disease are subepithelial deposits associated with?

A

Membranous nephropathy

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34
Q

Intrarenal: Glomerular Damage

What disease are subendothelial deposits associated with?

A

Membranoproliferative glomerulonephritis

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35
Q

Intrarenal: Glomerular Damage

What disease are mesangial deposits associated with?

A

IgA nephropathy

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36
Q

Intrarenal: Glomerular Damage

What are the clinical consequences of glomerular damage?

A

Nephritic or Nephrotic Syndrome

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37
Q

Intrarenal: Glomerular Damage

Nephritic Syndrome

A

Glomerular inflammation
proliferative changes and leukocyte infiltration
Proteinuria and edema are less severe than nephrotic syndrome

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38
Q

Intrarenal: Glomerular Damage

Nephrotic Syndrome

A

Podocyte Injury
Immune or non-immune causes
Structural and/or physiochemical alterations
Damage to glomerular membrane - protein leakage

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39
Q

Intrarenal: Glomerular Damage

Compare and contrats Nephritic and Nephrotic Syndrome

A

Nephrotic: No hematuria, oliguria, hypertension
Both have proteinuria (lower level in nephritic)

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40
Q

Intrarenal: Glomerular Damage

What is the clinical presentation of Nephritic Syndrome?

A

Hematuria
Oliguria with azotemia
Proteinuria
Hypertension

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41
Q

Intrarenal: Glomerular Damage

What are the most common causes of Nephritic Syndrome?

A

Immunologically-mediated glomerular injury
Acute postinfectious glomerulonephritis
Rapidly progressive glomerulonephritis (RPGN) which often leads to crescentic lesions

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42
Q

Intrarenal: Glomerular Damage

What is the clinical presentation of Nephrotic Syndrome?

A

Massive proteinuria - depletes serum albumin
Hypoalbuminemia - low albumin reduces osmotic pressure of blood
Generalized edema due to reduced osmotic pressure and compensatory aldosterone secretion (hypovolemia)
Hyperlipidemia and lipiduria

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43
Q

Intrarenal: Glomerular Damage

What are the causes of Nephrotic Syndrome?

A

Minimal-change disease
Membranous Nephropathy

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44
Q

Intrarenal: Glomerular Damage: Nephrotic Syndrome

Minimal-change disease

A

Due to glomerular damage, leakage across filtraion membrane
Lipoproteins accumulate in proximal convoluted tubules (visible lipid droplets and protein accumulations)
somep odocyte effacement - causes nephrotic syndrome

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45
Q

Intrarenal: Glomerular Damage: Nephrotic Syndrome

Minimal-change disease is most common in…

A

children

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46
Q

Intrarenal: Glomerular Damage: Nephrotic Syndrome

Membranous Nephropathy

A

Diffuse thickening of capillary walls (Ig deposits or self-antibodies)
Ig activates complement
Attack on podocytes allows protein leakage
Sudden onset

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47
Q

Intrarenal: Glomerular Damage: Nephritic Syndrome

What are the causes of Nephritic Syndrome?

A

Post-Streptococcal Glomerulonephritis
Goodpasture Syndrome
Crescentic Glomerulonephritis

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48
Q

Intrarenal: Glomerular Damage: Nephritic Syndrome

Post-Streptococcal Glomerulonephritis

A

Antibodies to steptococcal proteins will recognize glomerular proteins
activation of complement causes infiltration of neutrophils and other leukocytes
Immune response will also induce proliferation of cells in glomerulus (increased cellularity of glomerulus, deposits in subendothelial space, membrane, subepithelial space)

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49
Q

Intrarenal: Glomerular Damage: Nephritic Syndrome

Goodpasture syndrome

A

Renal failure with pulmonary hemorrhage
Parietal epithelial cells can transdifferentiate to produce replacement podocytes (immune response causes necrosis in glomerulus)

50
Q

Intrarenal: Glomerular Damage: Nephritic Syndrome

What causes Goodpasture Syndrome?

A

Antbodies against basement membrane components (Anti-GBM in kidney, which may recognize alveolar bm)

Anti-GBM antigen is in collagen IV; source of pulmonary hemorrhage

51
Q

Intrarenal: Glomerular Damage: Nephritic Syndrome

What is the clinical presentation of Goodpasture Syndrome?

A

Hemoptysis
Hematuria
Nephritic (and possibly nephrotic) syndrome

52
Q

Intrarenal: Glomerular Damage: Nephritic Syndrome

What is the treatment for Goodpasture Syndrome?

A

Plasmaphereis to remove antibodies
immunosuppression

53
Q

Intrarenal: Glomerular Damage: Nephritic Syndrome

Crescentic Glomerulonephritis

Rapidly progressive glomerulonephritis (RPGN)

A

Crescents form due to proliferation of parietal cells of Bowman’s membrane (induced my macrophages, monocyte chemotaxis)

54
Q

Intrarenal: Glomerular Damage: Nephritic Syndrome

Why is Crescentic Glomerulonephitis also known as rapidly progresisve glomerulonephritis?

A

Clinical syndrom - rapid loss of renal function

54
Q

Intrarenal: Glomerular Damage: Nephritic Syndrome

What are the 3 types of Crescentic Glomerulonephritis based on? What are they?

A

Immunological mechanisms
1. Anti-GBM antibody mediated disease (Goodpasture Syndrome)
2. Immune complex deposition (lupus)
3. Anti-neutrophil cytoplasmic antibodies (ANCAs) (idiopathic, systemic vasculitis)

55
Q

Intrarenal: Tubular Damage

Tubulointerstitial nephritis

A

Inflammation(nephritis) of interstitium (interstitial) and tubules(tubulo)

55
Q

Intrarenal: Tubular Damage: Pathways of Renal infection

Acute Pyelonephritis

A

Bacterial infection due to UTI

56
Q

Intrarenal: Tubular Damage: Pathways of Renal infection

Chronic Pyelonephritis

A

History of UTI
Fibrosis of pelvis and calyx

57
Q

Intrarenal: Tubular Damage: Pathways of Renal infection

Drug-induced inflammation

A

Edema and mononuclear infiltrate into interstitium
Penicillin derivatives, other antibiotics, NSAIDs, others

58
Q
A
59
Q

Intrarenal: Tubular Damage

Ionic Homeostasis

A

Balance between cations and anions

60
Q

Intrarenal: Tubular Damage

What is the purpose of Ionic Homeostasis?

A

maintain pH around 7.4
Concentrationsof ions maintain osmolarity
Ions necessary for function maintained at correct concentration

61
Q

Intrarenal: Tubular Damage

Exretion must be _ by intake to maintain balannce

A

matched

62
Q

Intrarenal: Tubular Damage

How much of your body weight is body water? What is it comprised of?

A

60% of body weight
breaks down to:
* 20% bw is ECF
* 40% bw is ICF

63
Q

Intrarenal: Tubular Damage

What is the ECF? What are the major cations and anions?

A

Plasma + interstitial (filtrate of plasma; no cells or large proteins) (Extracellular fluid)
Cation: Na+
Aniona: Cl- and HCO3-

64
Q

Intrarenal: Tubular Damage

What is the ICF? What are the major cationd and anions?

A

Intracellular fluid
Cations: K+ and Mg2+
Anions: proteins and organic phosphates (ATP, ADP, AMP)

65
Q

Intrarenal: Tubular Damage

Water Intoxication

Water poisoning/Fatal hyponatremia

A

Drink so much water it becomes toxic - kidney cant remove fluid fast enough

Urine excretion can be increased to 16 mL/min (usually 1 ml/min) when large quantities of hypotonic fluid are ingested
If ingestion exceeds this, or continues for too long, cells will swell due to water uptake to cope with Hypotonic ECF

66
Q

Intrarenal: Tubular Damage

What are the symptoms of water intoxication?

A

Swelling of CNS neurons
Convulsions, coma (can kill)

67
Q

Kidney Injury

What is the most common cause of acute renal failure? Why?

A

Acute Kidney Injury
Rapid reduction of renal function, including output <400 ml/day (oliguria to anuria)
50% of acute renal failure occurs in hospital patients

68
Q

Kidney Injury

What evidence could you find of tubular injury?

A

glomerular, interstitial, vascular injury

69
Q

Kidney Injury

What are the causes of Acute Kidney Injury?

A

Ischemia
Direct Toxic Injury
Inflammation
Urinary Obstruction

70
Q

Kidney Injury

What causes ischemia in AKI?

A

Malfunction of intrarenal blood vessels
Thomboses
Decreased blood volume

70
Q

Kidney Injury

What causes urinary obstruction in AKI?

A

Tumors, prostatic hypertrophy, blood clots

71
Q

Kidney Injury

Pathogenesis of AKI

A

Tubule Cell injury (Toxic/Ischemic Injury)
Distrubed Blood flow

72
Q

Kidney Injury

Tubule Cell Injury: Toxic Injury

A

Cells are more sensitive due to higher metabolic requirements, high absorption rates, and concentration capacity

73
Q

Kidney Injury

Tubule Cell Injury: Ischemic Injury

A

Tubules cells are more sensitive to lack of nutrients
ischemia causes vasoconstriction

74
Q

Kidney Injury

Disturbed Blood Flow

A

Hemodynamic alterations affect GFR

75
Q

Kidney Injury

What is the treatment for AKI?

A

Prevent further damage (address cause)
Antibiotics - prevent secondary infections
Diuretics - flush out the kidneys
Dialysis

76
Q

Kidney Injury

How is the damage distributed in AKI?

A

Proteins, lipids, blood cells acculate on the inner aspect of the tube
Form casts that can be passed into the urine
Necrosis occurs in areas most impacted by damage

77
Q

Kidney Injury

How do you differentiate the connvoluted tubules?

A

DCT: Less esosinophilic
PCT: Visible brush border
Both: Cuboidal Cells

78
Q

Chronic Kidney DIsease

What is the difference between Chronic Kidney Disease and AKI?

A

Chronic Kidney Disease: Irreversible loss of tubular cells
AKI: can resolve through regeneration

79
Q

Chronic Kidney DIsease

What is the cause of chronic kidney disease?

A

Most common cause is diabetes mellitus
Other common causes include hypertension and glomerulonephritis

endpoint of all chronic renal parenchymal diseases

80
Q

Chronic Kidney DIsease

What are the markers of kidney damage?

A

Alterations in blood
urine composition

81
Q

Chronic Kidney DIsease

What is the treatment for Chronic Kidney Disease?

A

Address underlying cause
Changes in diet, lifestyle to prevent damage
Serious: Dialysis, transplant

82
Q

Chronic Kidney DIsease

Chronic Kidney Disease

A

Irreversible loss of tubular cells
Significntly decreased GFR and/or albuminuria for 3 months

83
Q

Chronic Kidney DIsease

What are the clinical manifestations of kidney damage?

A

altered kidney functions that affect:
* Sodium and potassium homeostasis
* Water balance
* Acid-base balance
* Urea excretion

84
Q

Chronic Kidney DIsease

How does kisney damage affect sodium potassium homeostasis?

A

Excess Na+ expands intravascular volume
Hypertension and congestive heart failure

85
Q

Chronic Kidney DIsease

How does kidney damage affect urea excretion?

A

Reduced excretion increases BUN and serum creatinine, produces uremia

BUN = blood urea nitrogen

86
Q

Chronic Kidney DIsease

What are clinical symptoms of kidney damage?

A

Dehydration, edema, hyperkalemia
Hyperphosphatemia, hypocalcemia, bone/parathyroid effects
anemia
Hypertension, congestive heart failure, cardiomyopathy, pulmonary edema, uremic pericarditis
Nausea and vomiting, GI bleeds, inflammation of the esophagus, stomach, colon
Skin: sallow, pruritic, dermatitis

87
Q

Kidney Damage

Uremia

A

Increases levels of urea in the blood

88
Q

Kidney Damage

What are the symptoms of Uremia?

A

Decreased appetite
Fatigue
Neurological symptoms (confusion, coma)
Skin excretion (uremic frost)

89
Q

Kidney Damage

What causes uremia?

A

Accumulation of nitrogenous waste products due to kidney failure
Hypotension
dehydration
trauma (increased protein catabolism)

90
Q

Kidney Damage

What are other consequences of Uremia?

A

Kidneys no longer activate vitamin D
Necessary for calcium/phosphate absorpion

91
Q

Renal Osteodystrophy

Renal Osteodystrophy

A

Lack of vitamin D reduces intestinal Ca2+ absorption

92
Q

Renal Osteodystrophy

What is the mechanism of Renal Osteodystrophy?

A

Low plasma Ca2+ causes parathyroid hyperplasia
PTH increases oteoclast activity
Secondary hyperparathyroidism causes bone calcium depletion

93
Q

Obstructive Uropathy

What are the most common sites of Kidney Stones?

A

Collecting system
Renal pelvis and calcyes

94
Q

Obstructive Uropathy

What are the causes of kidney stones?

A

Genetics
Dehydration
Dietary Intake
Hormonal imbalance (parathyroid tumor)

95
Q

Obstructive Uropathy

What are the 4 types of kidney stones?

A

Calcium (75%)
Uric Acid (<10%)
Cystine (1%)
Infection (15%)

96
Q

Obstructive Uropathy

Kidney Stones: Calcium

A

75% of kidney stones are calcium
oxalate and/or phosphate salts

97
Q

Obstructive Uropathy

Kidney stones: Uric Acid

A

<10% of kidney stones
25% of gout/hyperuricemia patients
most are idiopathic

98
Q

Obstructive Uropathy

Kidney Stones: Cystine

A

1% of kidney stones
Children with hereditary cystinuria

99
Q

Obstructive Uropathy

Kidney Stones: Infection

A

15% of kidney stones
Bacteria cleave urea
* Proteus or providencia species
* produces ammonia - caused urine to become alkaline - favors salt deposition - Struvite NH4MgPO4.6H2O - apatite Ca5(PO4)3(OH)2

100
Q

Obstructive Uropathy

What are the consequences of the obstruction of kidney stones?

A

Damage typically seen in tubules
Causes increased intrarenal pressure (will damage tissue, infection or abscess can occur behind stone)
Hypertension due to renin production

101
Q

Obstructive Uropathy

What causes pain from kidney stones?

A

Due to distension of renal capsule, renal pelvis or ureters
Damage to these structures can cause ureters

102
Q

Obstructive Uropathy

Hydronephrosis

A

Expansion of pelvis and calcyes due to obstruction in ureters or further out

Urine backs up into kidneys

103
Q
A
104
Q

Obstructive Uropathy

What causes hydronephrosis?

A

Calculus can block ureters
Will compress parenchyma and damage it (tubules first, then glomeruli; atrophy and fibrosis)

105
Q

Obstructive Uropathy

Hydronephrosis: Unilateral Blockage

A

Blockage in ureter

106
Q

Obstructive Uropathy

Hydronephrosis: Bilateral blockage

A

Blockage in bladder or urethra

107
Q

Obstructive Uropathy

How do you treat kidney stones?

A

Pain magement
Prevent dehydration (water and other fluids)
Use shock waves to break up the stone
Stent in ureter to maintain patency
Prevent new stones from forming (depends on type of stone)

108
Q

Obstructive Uropathy

How can allopurinol be used to treat kidney stones?

A

Inhibits purine catabolism to reduce uric acid production

109
Q

Postrenal

Actue cystitis

A

Neutrophil infiltrate
Inflammation of bladder

110
Q

Postrenal

Chronic Cystitis

A

Mononuclear infiltrate (macrophages and T cells)
Inflammation of bladder

111
Q

Postrenal

Types of cystitis (bladder inflammation)

A

Bacterial infection (or viral)
Hemorrhagic
Interstitial
Malakoplakia
Polypoid

112
Q

Postrenal

Hemorrhagic cystitis

A

Side-effect of cytotoxic chemotherapeutics
can be due to adenovirus infection

113
Q

Postrenal

Interstitial Cystitis

A

Pain when bladder fills
Other symptoms: Urgency, hematuria, dysuria

114
Q

Postrenal

Malakoplakia Cystitis

A

Defects in phagocytic cells (undigested bacterial components accumulate)

115
Q

Postrenal

Polypoid Cystitis

A

May look like papillomatous cancer but due to submucosal edema

116
Q

Postrenal

What are the most common species to cause Cystitis?

A

E. coli (most common), Proteus, Klebsiella, Enterobacter

117
Q

Postrenal

What are the predisposing factors of cystitis?

A

Bladder stones
Obstruction
Diabetes mellitus
Immune defificency

118
Q

Postrenal

What are the triad of symptoms of cystitis?

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

Mechanism of Disease (11 decks)

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