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Test 4 Advanced Pathophysiology Dr. Gonzalez > Renal Disorders > Flashcards

Renal Disorders Flashcards

1
Q

Nephrolithiasis is also known as

A

kidney stones or renal calculi

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2
Q

The presence of renal stones within the renal pelvis and/or calyces is?

A

Nephrolithiasis

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3
Q

Kidney stones may be present where?

A
  • renal pelvis
  • calyces
  • ureters
  • urinary bladder
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4
Q

The first occurence of kidney stones is usually before the age of?

A

50

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5
Q

Risk factors for kidney stones are: (10)

A
  • age
  • male gender
  • fluid intake
  • caucasian
  • diet
  • HTN
  • atherosclerosis
  • metabolic syndrome
  • obesity
  • DM type 2
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6
Q

Renal calculi are made up of: (4)

A
  • calcium
  • struvite
  • uric acid
  • cystine
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7
Q

Cystine is?

A

an amino acid found in most proteins

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8
Q

What are the most common renal calculi made of?

A

Calcium stones are the most common and are frequently calcium oxalate or calcium phosphate

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9
Q

Why do kidney stones occur?

A
  • idiopathic hypercalciuria

- in the setting of hyperparathyroidism

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10
Q

What results in an increase in osteoclastic activity?

A

hyperparathyroidism

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11
Q

What are the bone cells which break down bone and release calcium into the blood?

A

Osteoclasts

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12
Q

What is the second most common type of renal calculi?

A

Strivite

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13
Q

What is struvite made of?

A

magnesium, ammonium, and phosphate salts

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14
Q

What causes struvite renal calculi?

A

They tend to result from chronic UTIs with urease producing bacteria such as proteus and pseudomonas

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15
Q

How are struvite renal calculi produced?

A

The urease produced by these bacteria breaks down the urea in the urine to the salts that compose struvite stones

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16
Q

What type of renal calculi are the most troubling?

A

struvite stones

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17
Q

Why are struvite stones the most troubling?

A

These stones are the most troubling ones because they frequently cause complications with intractable urinary tract infections, pain, bleeding, and abscess.

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18
Q

What is the third most common kidney stone?

A

Uric acid

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19
Q

How are uric acid stones produced?

A

Uric acid results from the breakdown of purines (DNA).

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20
Q

Who usually suffers from uric acid kidney stones?

A

These types of stones tend to form in persons with excess purine intake or persons with gout.

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21
Q

What is the most commonly occuring kidney stone in children?

A

Cystine stones

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22
Q

What is the least common type of kidney stone for adults?

A

Cystine stones

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23
Q

What is the pathophysiology of nephrolithiasis?

A
  1. begins with the oversaturation of urine with ions (calcium, magnesium, ammonium, etc.)
  2. The cations and anions bond with one another and form salts which precipitate into crystals.
  3. The crystals then form stones which pass into the ureter and cause excruciating flank pain (renal colic) and obstruction.
  4. The obstruction causes the urine to back up into the kidney resulting in hydronephrosis and renal failure.
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24
Q

What size stone will have a 50% chance of passing without any complications?

A

5mm or less

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25
Q

Stones that are what size will likely not pass spontaneously?

A

1cm

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26
Q

Specific risk factors for kidney stones: Gout which results from?

A

an accumulation of uric acid

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27
Q

Specific risk factors for kidney stones: Dehydration…

A

whose link to the pathophysiology of nephrolithiasis is unknown

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28
Q

Specific risk factors for kidney stones: High protein diets

A

resulting in an increase in purine intake

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29
Q

Specific risk factors for kidney stones: High sodium diets

A

predisposes the individual to increased calcium excretion and therefore to calcium stone formation

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30
Q

Specific risk factors for kidney stones: HTN

A

has a role in the formation of renal calculi but the association is not clear

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31
Q

Clinical manifestations of renal calculi?

A
  • flank pain that radiates to the groin
  • anuria (bilateral obstruction)
  • azotemia (bilateral obstruction)
  • hematuria
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32
Q

Used in medical terminology to refer to a localized area of disease

A

focal

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33
Q

in relationship to glomerular disorders it means that < 50% of glomeruli are affected by the disorder

A

focal

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34
Q

Refers to the more widespread involvement of glomerular injury (usually > 50% affected)

A

diffuse

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35
Q

used to describe the condition of hypercellularity of the glomeruli

A

proliferative

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36
Q

refers to the thickening of the glomeruli basement membrane

A

membranous

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37
Q

involves only the kidney and the cause of the disease is directly related to the kidney

A

primary glomerular disease

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38
Q

the injury is caused by a mechanism outside of the kidney which is what occurs with lupus or diabetes

A

secondary glomerular disease

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39
Q

There are three main patterns of injury seen in glomerular disorders -

A
  • hypercellularity
  • leukocytic infiltration
  • formation of crescents
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40
Q

an increased number of cells in the glomerulus

A

hypercellularity

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41
Q

cellular proliferation of the mesangial or endothelial cells

A

hypercellularity

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42
Q

results from accumulation of cells made of proliferating epithelial cells and infiltrating leukocytes

A

formation of crescents

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43
Q

what tends to occur after an immune or inflammatory response

A

formation of crescents

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44
Q

results in a thickening of the capillary walls of the glomerulus

A

basement membrane thickening

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45
Q

what is the accumulation of homogeneous and eosinophilic cells in the lumen of the glomerular capillaries

A

hyalinosis

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46
Q

when extensive - it obliterates the glomerular capillary lumens

A

hyalinosis

47
Q

usually occurs as a result of capillary wall injury and it is usually the end result of glomerular damage

A

hyalinosis

48
Q

this is commonly seen with focal segmental glomerulosclerosis

A

hyalinosis

49
Q

what is the accumulation of extracellular collagenous matrix

A

sclerosis

50
Q

it may be limited to the mesangial cells or involve the capillary loops of the glomerulus or both

A

sclerosis

which is what happens with diabetic glomerulosclerosis

51
Q

this may obliterate capillary lumens in the glomeruli and result in the formation of adhesions in the bowman’s capsule

A

sclerosis

52
Q

is an abrupt reduction in renal function with oliguria

A

acute kidney injury

53
Q

what is the mortality rate of AKI?

A

50-80%

54
Q

What percent of hospitalized patients have AKI?

A

5%

55
Q

it is usually reversible if the underlying cause is treated

A

AKI

56
Q

There are 3 stages of AKI.

Describe stage 1

A

1 - creatinine 1.5-1.9 times higher than baseline or greater than or equal to 0.3mg/dL increase in creatinine

57
Q

There are 3 stages of AKI. Describe stage 2

A

2 - a creatinine of 2-2.9 times higher than the baseline

58
Q

There are 3 stages of AKI. Describe stage 3.

A

3 - creatinine of 3.0 times higher than the baseline or an
increase in serum creatinine to ≥ 4.0 mg/dL or the initiation of renal replacement
therapy or in person less than 18 years old a decrease in eGFR to < 35ml/minute
per 1.732

59
Q

There are three categories of AKI and they include:

A

pre-renal, intra-renal or intrinsic, and
post-renal. These terms are very descriptive of the etiology and the pathophysiology of
AKI.

60
Q

caused by impaired blood flow to the kidney resulting in a decreased
GFR.

A

Pre-renal AKI

61
Q

Anything which decreases renal perfusion can cause a pre-renal AKI. Etiologies
include:

A

Vasoconstriction of renal arteries from medications or shock states.
• Hypotension
• Hypovolemia
• Hemorrhage
• Inadequate cardiac output i.e. heart failure
• NSAIDS
• Renal artery stenosis

62
Q

is the most common cause of AKI.

A

Pre-renal AKI

63
Q

Laboratory findings consistent with

AKI include

A

a FeNa of < 1% and a BUN:Creatinine ratio of > 20

64
Q

A fractional excretion of sodium (FeNa) is used to

A

evaluate an acute kidney injury and to

differentiate between a pre-renal and acute tubular necrosis

65
Q

It is a calculated measure

based off the serum sodium, serum creatinine, urine sodium and urine creatinine.

A

A fractional excretion of sodium (FeNa)

66
Q

It is

reported as a percentage and is a marker of renal sodium excretion.

A

A fractional excretion of sodium (FeNa)

67
Q

A FeNa which is less than 1% indicates

A

that the kidneys are conserving sodium and is

indicative of a pre-renal AKI.

68
Q

A FeNA which is greater than 2% indicates

A

that the

kidneys are wasting sodium and is consistent with an acute tubular necrosis.

69
Q

Values
between 1-2% are indeterminate and are not helpful in differentiating between the two
disease processes.

A

A fractional excretion of sodium (FeNa)

70
Q

may be used to evaluate the etiology of an acute renal injury.

A

The BUN:Creatinine ratio

71
Q

The ratio is a comparison between serum BUN and creatinine

A

The BUN:Creatinine ratio

72
Q

It can be used to

differentiate between a pre-renal AKI or intra-renal AKI

A

The BUN:Creatinine ratio

73
Q

A ratio that is greater than 20 is

consistent with a pre-renal acute kidney injury (AKI).

A

The BUN:Creatinine ratio

74
Q

is caused by an issue which has impaired renal function at the cellular
level in the kidney

A

Intra-renal AKI

75
Q

The two main causes of intra-renal AKI are:

A

Inflammatory conditions and acute tubular necrosis

76
Q

What are some inflammatory conditions that cause intra-renal AKI

A

glomerulonephritis, vasculitis, drug induced

toxicity such as aminoglycosides

77
Q

results in a severe necrosis of tubular epithelial cells.

The cells slough off and collect in the tubule and cause an obstruction

A

Acute Tubular necrosis (ATN)

78
Q

This
obstruction causes an increase in tubular pressure that subsequently leads to a
decreased GFR.

A

acute tubular necrosis

79
Q

The decrease in the GFR causes the afferent arteriole to vasoconstrict
and this decreases GFR even further. The increased tubular pressure also leads to back
flow of fluid into the renal interstitial tissue

A

acute tubular necrosis

80
Q

What you will see clinically is a rising
creatinine and BUN. The creatinine will rise until it peaks. I have seen it go as high as
10 and then it will come down. When it starts coming down these individuals will
begin to diuresis and they can easily get dehydrated. Prior to this they are at risk for
volume overload. During the time the creatinine is rising, the individual is at risk for
electrolyte imbalances such as hyperkalemia, hyperphosphatemia, hypocalcemia etc.
Anytime the kidney is injured regardless of the cause, the person is at risk for
electrolyte and acid base imbalances that you see in CKD and potentially other
complications too.

A

acute tubular necrosis

81
Q

Causes of ATN include

A

sepsis, post-surgical complications,

obstetrical complications, and medications

82
Q

Any pre-renal etiology can be so profound

that it progresses to

A

ATN - acute tubular necrosis

83
Q

ATN caused by ? is the most common cause of

intra-renal injuries.

A

ischemia

84
Q

caused by a urinary tract obstruction such as bladder outlet obstruction.

A

Post-renal AKI

85
Q

may occur as a result of prostatic hyperplasia or ureteral

obstruction from a urinary stone

A

A bladder outlet obstruction

86
Q

An obstruction increases retrograde pressure and causes

an

A

ATN - acute tubular necrosis

87
Q

Regardless of the origin of ARF, all forms of acute renal failure, if left
untreated, will all result in

A

ATN - acute tubular necrosis

88
Q

Clinical manifestations of AKI are dependent upon the cause. Manifestations include:

A

• Oliguria, anuria
• Fatigue, edema, dyspnea
• Mental status changes secondary to uremia
• Electrolyte imbalances include hyperkalemia, hyponatremia.
• Metabolic acidosis
• BUN:Creatinine Ratio will be > 20 in a pre-renal AKI. It will be normal in intra-renal
AKI.
• FeNa will be < 1% in pre-renal AKI and > 2% in an ATN.
• Muddy Brown Cast cells are seen in the UA with ATN.

89
Q

progressive and irreversible loss of nephron function.

A

CKD - chronic kidney disease

90
Q

There are five stages of

A

CKD

91
Q

The five stages are defined by the

A

GFR

92
Q

CKD Stage I is defined by

A

a GFR of ≥ 90 ml/min.

a. These people are usually asymptomatic

93
Q

• CKD Stage II is defined by

A

a GFR of 60-80 ml/min.
a. These individuals experience an increase in PTH, early bone disease,
increasing plasma creatinine and urea. They may have subtle hypertension.

94
Q

• CKD Stage III is defined by

A

a GFR of 30-59 ml/min.
a. These individuals have erythropoietin deficiency, experience anemia, and have
an increase in creatinine and urea. They will have mild HTN.

95
Q

CKD Stage IV is defined by

A

a GFR of 15-29 ml/min.
a. These individuals experience increased triglycerides, metabolic acidosis,
hyperkalemia, sodium and water retention and elevated BUN/creatinine.
Additional symptoms include moderate HTN, hyperphosphatemia, and anemia.

96
Q

• CKD Stage V is defined by

A

a GFR of < 15 ml/min or the need for hemodialysis. This
results in uremia. They will also experience severe HTN, anemia and
hyperphosphatemia.

97
Q

CKD usually occurs over a number of years as the internal structures of the kidneys are
slowly damaged by one or more of the following processes:

A

Diabetes is the most common cause.
• HTN is the second most common cause.
• Glomerulonephritis is the third most common cause.
• Polycystic kidney disease
• Obstructive problems such as renal stones

98
Q

CKD begins with a chronic injury to the kidney which causes

A

an irreversible loss of

nephrons

99
Q

The loss of nephrons causes an increase in

A

glomerular filtration pressure in
remaining nephrons. This increase in pressure causes hyperfiltration (HTN at the
nephron) of the remaining nephrons.

100
Q

This causes more nephrons to fibrose and scar

resulting in

A

the loss of more nephrons. This will ultimately lead to uremia and the clinical
manifestations of CKD.

101
Q

Eventually the individual will become oliguric and anuric. The
clinical manifestations include:

A
  • Uremia
  • Anemia
  • Fluid and electrolyte imbalances
  • secondary hyperparathyroidism
  • decreased synthesis of vitamin D
  • hypocalcemia
  • Osteodystrophy
  • normocytic anemia
  • HTN
  • altered mental status
  • Insulin resistance
  • CVD
  • Impaired platelet function
102
Q

is the accumulation of urea and other toxins which accumulate due to the
decrease in GFR and renal function.

A

Uremia

103
Q

secondary to decrease erythropoietin levels. This can lead to left ventricular
hypertrophy.

A

Anemia

104
Q

They include:
a. Hyperkalemia is common in late stages when the patient is oliguric. In early
stages potassium excretion is maintained.
b. Fluid volume deficit and Hyponatremia- during the early stages sodium and
fluid wasting occurs secondary to lack of the kidney’s ability to concentrate
urine.
6
c. Fluid overload and hypernatremia occur in late stages as the patient becomes
oliguric. Sodium is not excreted and accumulates as does fluid.
d. Hyperphosphatemia occurs due to a decreased excretion of phosphorus.
e. Hypocalcemia occurs because calcium has an inverse relationship to
phosphorus. A decreased production of the active form of vitamin D
(calcitriol). This is needed for the absorption of calcium in the gut.
f. Metabolic Acidosis occurs because of the kidney’s inability to reabsorb urinary
bicarb (HCO3) or excrete H+

A

Fluid and electrolyte imbalances are common.

105
Q

occurs to compensate for the low calcium levels
which are secondary to the hyperphosphatemia. Hyperphosphatemia occurs because
the kidneys are not able to excrete phosphorus. Most of phosphorus in the body comes
from the diet. Remember that phosphate binds with calcium and they have an inverse
relationship. When phosphorus is elevated, it binds more calcium which then
decreases the calcium level. This is the trigger for PTH secretion.

A

Secondary hyperparathyroidism

106
Q

(calcitriol), therefore calcium absorption

is impaired.

A

Decreased synthesis of activated vitamin d

107
Q

results from the secondary hyperparathyroidism. Remember PTH
causes an increase in osteoclastic activity, which causes the breakdown of bone.
Osteodystrophy is defective bone formation which leads to osteoporosis. The
metabolic acidosis associated with CKD also contributes to the development of
osteodystrophy.

A

Osteodystrophy

108
Q

commonly occurs and is due to a decreased secretion of

erythropoietin from the kidney.

A

a normocytic anemia

109
Q

occurs or worsens because failing kidneys secrete more renin. This results in
more angiotensin II and vasoconstriction.

A

HTN

110
Q

can occur from the increased levels of urea and other uremic

toxins. This usually will not be seen unless the BUN is > 100.

A

Altered mental status

111
Q

is common in CKD. Hyperparathyroidism decreases insulin
sensitivity and impairs glucose tolerance. As the kidney function decreases it is not
able to clear adiponectin and leptin which can contribute to the insulin resistance. Also
the failing kidney is not able to degrade insulin so insulin’s half life is prolonged.

A

Insulin resistance

112
Q

is common in CKD. They tend to have high triglyceride levels, low
HDLs and high LDLs.

A

Dyslipidemia

113
Q

is the main cause of death in persons with CKD. This is
secondary to the dyslipidemia that they experience, anemia, increase release or renin
and vascular calcification. All of these increase the risk for ischemic heart disease.

A

Cardiovascular disease

114
Q

is caused by the uremic environment. Platelets are not able

to aggregate in a uremic environment.

A

Impaired platelet function

Test 4 Advanced Pathophysiology Dr. Gonzalez (4 decks)

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