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ACUTE RENAL FAILURE Flashcards

1
Q

define acute kidney injury

A
  • is a rapid rise in blood urea nitrogen (BUN) and creatinine over several hours to days
  • a rise in creatinine and a decrease in renal function or glomerular filtration rate.
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2
Q

In rhabdomyolysis or contrast-induced renal failure, it may develop IN ………….

A

several hours.

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3
Q

In aminoglycoside toxicity or poststreptococcal glomerulonephritis, it may develop in

A

several weeks.

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4
Q

Renal insufficiency means renal failure, but not to

A

the point of needing dialysis

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5
Q

azotemia means

A

buildup of azole groups or nitrogen in the blood

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6
Q

Uremia (which means urea in the blood) describes

A

very severe renal failure in which dialysis is needed to save life

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7
Q

Clinical presentation of ACUTE RENAL FAILURE

A

1– Severe acidosis, mental status changes, hyperkalemia, and fluid overload
2– Anemia, hypocalcemia, and possible pericarditis
3– Bleeding diathesis due to platelet dysfunction

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8
Q

Uremia does not necessarily mean

A

chronic renal failure as from diabetes

or hypertension,

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9
Q

it is possible to become uremic in as little as 1–2 weeks with a severe illness such as

A

tumor lysis syndrome or rhabdomyolysis

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10
Q

AKI is also classified as

A

prerenal, postrenal, or intrarenal to determine the site of the defect.

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11
Q

Prerenal azotemia means

A

decreased perfusion of the kidney

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12
Q

Postrenal azotemia means

A

decreased drainage from the kidney or decreased forward flow of urine.

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13
Q

Intrarenal azotemia means

A

a tubular or glomerular problem, and the kidney itself is defective.

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14
Q

Diagnostic Tests of ACUTE RENAL FAILURE

A
  • BUN becomes abnormally elevated.
  • can be falsely elevated even when renal function is normal, in response to increased protein load in the diet or GI bleed. This is also from increased catabolism. The BUN is derived from protein waste products; blood in the gut acts like a big protein meal
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15
Q

BUN will improve after

A

a session of dialysis

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16
Q

The BUN can be falsely low when there is

A

liver disease, malnutrition, or SIADH.

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17
Q

The BUN level corresponds to the degree of

A

renal failure, the higher the BUN, the worse the kidney function.

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18
Q

what is Creatinine ?

A

a metabolic product of skeletal muscle, is our main measure of renal function.

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19
Q

Creatinine clearance is our closest approximation of

A

glomerular filtration rate (GFR)

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20
Q

Creatinine clearance slightly overestimates GFR because

A

there is some tubular secretion of creatinine.

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21
Q

Creatinine can be falsely low because of

A

decreased muscle mass

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22
Q

Creatinine needs some time to

A

rise.

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23
Q

if the patient becomes anuric, the creatinine will rise only at a rate of

A

0.5–1.0 point per day

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24
Q

This rise will be faster if the body muscle mass

A

is greater

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25
Q

if the creatinine goes from 1 to 3 over 2 days in a patient with renal injury, this is consistent with

A

nonfunctioning kidneys

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26
Q

define Prerenal Azotemia

A
  • a form of renal insufficiency caused by diminished perfusion of the kidney
  • The kidney itself is normal
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27
Q

If the kidney could receive adequate perfusion,

the BUN and creatinine would

A

normalize.

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28
Q

The causes of prerenal azotemia include

A

1- hypovolemia on any basis (dehydration, burns, poor oral intake, diuretic, vomiting, diarrhea, sweating, hemorrhage),
2-hypotension on any basis (septic shock, cardiogenic shock, anaphylactic shock),
3-and third spacing of fluids such as peritonitis, osmotic diuresis, or low aldosterone states such as Addison disease

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29
Q

Addison disease results in

A

intravascular volume depletion, leading to diminished tissue perfusion.

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30
Q

Diminished perfusion from a decrease in cardiac output also results in

A

prerenal azotemia

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31
Q

Although there may be total body fluid overload with significant edema, all that matters in terms of renal function is

A

1-how much fluid is still in the vascular space and

2-how much can provide meaningful perfusion of the kidney

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32
Q

With severe CHF, constrictive pericarditis, or coarctation of the aorta, there may be

A

edema and fluid overload

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33
Q

The first clue to the diagnosis of prerenal azotemia is

A

BUN:creatinine ratio of 20:1

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34
Q

what are the other clues to the diagnosis of prerenal azotemia?

A

low urine sodium and low fractional excretion of sodium (FeNa <1%)
- because the kidney perceives the body as being volume-depleted (hence, there will be a vigorous sodium and water reabsorption by the kidney).

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35
Q

low urine sodium and low fractional excretion of sodium results in

A

a very high urine osmolality, because the kidney attempts to retain all the water it can in the kidney, and therefore excretes very concentrated urine

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36
Q

Concentrated urine has

A

a high specific gravity (>1.010) and high urine osmolality (>500).

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37
Q

Low albumin states also lead to

A

decreased renal perfusion

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38
Q

diagnosis of prerenal azotemia is

A

BUN:creatinine ratio rises to 20:1, urine sodium is low, and the urine osmolality is high

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39
Q

Renal artery stenosis, especially if bilateral, results in

A

high BUN and creatinine with a high BUN:creatinine ratio

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40
Q

Although systemic BP may be markedly elevated, the result is still a form of

A

prerenal azotemia.

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41
Q

There is markedly diminished renal perfusion because of the obstruction

A

in the renal artery

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42
Q

The systemic BP does not matter; all that matters is

A

how much is getting to the kidney

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43
Q

renal artery stenosis functions like

A

hypotension

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44
Q

renal artery stenosis effect is greatly exaggerated with the use of

A

ACE inhibitors, which markedly diminish renal perfusion. because of the extremely high aldosterone state

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45
Q

define Hepatorenal syndrome

A

renal failure based entirely on the presence of hepatic failure. The kidneys are normal

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46
Q

The rise in BUN and creatinine is believed to be due to an

A

intense vasoconstriction of the afferent arteriole, causing decreased renal perfusion

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47
Q

Because the defect is at the afferent arteriole, lab numbers are consistent with prerenal azotemia like

A

1-high BUN:creatinine ratio >20:1.
2-Urine sodium is low (<10) and fractional excretion of sodium <1%
3-Intrinsic renal disease should be excluded to make a diagnosis.
4-No improvement in renal failure after 1.5 L of colloid, like albumin, is diagnostic of hepatorenal syndrome

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48
Q

Treatment of Hepatorenal syndrome is

A

1-correction of the underlying liver disease.
2-Midodrine, an alpha agonist,
3-and octreotide may be beneficial,
4-but the best treatment is liver transplantation

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49
Q

ACE inhibitor–induced renal failure is caused by

A

vasodilation of the efferent arteriole.

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50
Q

Angiotensin has a significant vasoconstrictive effect on

A

the efferent arteriole

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51
Q

ACE inhibitors block this vasoconstrictive effect, causing

A

a decreased GFR that is usually transient

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52
Q

in the elderly, diabetics, hypertensives, or patients with baseline renal disease such as from myeloma, an ACE inhibitor can produce

A

a marked decrease in renal function.

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53
Q

if there is underlying renal insufficiency, there can be a

rise in

A

BUN and creatinine after initiating an ACE inhibitor

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54
Q

In patients with bilateral renal artery stenosis, observe for

A

severe decline in renal function after an ACE inhibitor has been initiated.

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55
Q

Despite the ability of ACE inhibitors to potentially worsen renal function, their overall effect on the kidney is to

A

diminish the rate of progression to uremia and renal failure

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56
Q

This beneficial effect is most likely secondary to the decrease in

A

intraglomerular hypertension

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57
Q

ACE inhibitors and angiotensin receptor blockers decrease

A

hypertension inside the glomerulus

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58
Q

ACE inhibitors decrease proteinuria by

A

35–45%.

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59
Q

ACE inhibitors produce a brief decrease in

A

GFR in the short-term

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60
Q

with a long-term beneficial effect on decreasing

A

proteinuria and the rate of progression of renal failure. This is particularly true in patients with diabetes.

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61
Q

Postrenal azotemia is caused by any decrease in

A

the outflow of urine

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62
Q

One cannot get renal failure by the obstruction of a single kidney if a patient has both kidneys in place, i.e., a large stone in one ureter cannot cause

A

renal failure because creatinine does not rise if there is loss of only one kidney.

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63
Q

A small stone or clot in the bladder can obstruct both …………, and this can cause …………

A

kidneys

postrenal azotemia.

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64
Q

Other causes of postrenal azotemia include

A

-bladder cancer, prostate hypertrophy/cancer, bilateral ureteral disease e.g., retroperitoneal fibrosis, neurogenic bladder, or any other cause of bilateral obstructive disease.

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65
Q

Strictures can cause this problem but only if they are ……………. in location.

A

bilateral

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66
Q

The complete obstruction of a single kidney does not cause renal failure because

A

only 35% of one kidney is needed in order to live

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67
Q

Creatinine will begin to rise only 70–80% if renal function has been

A

lost

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68
Q

Thus, more renal function is lost as one goes from

creatinine……………than from creatinine………….

A

1 to 2

2 to 10.

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69
Q

Patients usually have a preceding history of obstructive symptoms followed by

A

sudden onset of oliguria or anuria.

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70
Q

Neurologic causes such as MS, spinal cord lesion, and neuropathy may lead to

A

poor function of the urinary bladder and obstruction.

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71
Q

what is the diagnosis of Postrenal Azotemia

A
  • Initially, BUN and creatinine will elevate in a ratio 20:1 as it does with prerenal azotemia.
  • There will also be a low fractional excretion of sodium (FeNa) and low urine sodium.
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72
Q

When the obstruction continues for such a long time that there is permanent damage to the kidney and the kidney tubule cells die, then the BUN:creatinine ratio
will

A

lower to 10:1, as is seen in acute tubular necrosis (ATN). Early diagnosis is, therefore, essential. Complete recovery is possible until 10–14 days of obstruction.

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73
Q

ATN is the most common cause of ……… (intrinsic) in hospitalized patients.

A

AKI

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74
Q

The diagnosis of postrenal azotemia is determined by finding

A

1-a distended bladder on examination,
2-bilateral hydronephrosis on renal sonogram or CT scan,
3-or by finding large volumes of urine in the bladder after passing a Foley urinary catheter

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75
Q

After urinating (voiding), there should be no more than ………. of urine left in the bladder. If this post-void residual is markedly elevated, it implies an…………… to the flow of urine out of the bladder.

A

50 mL

obstruction

76
Q

Treatment is based on relieving the cause of the

A

obstruction

77
Q

define Acute tubular necrosis

A

acute renal failure on the basis of tubular damage (as opposed to glomerular damage), or simply decreased perfusion of the kidney or drainage out of the kidney.

78
Q

About 85% of acute renal failure is secondary to intrinsic renal disease such as

A

ATN

79
Q

ATN is caused by

A

hypoperfusion of the kidney
leading to such severe ischemia that there is cellular death or by a toxic injury to the kidney such as aminoglycoside toxicity or from amphotericin (caused by sepsis or post-cardiac/aortic surgery).

80
Q

ATN often occurs from a combination of

A

toxic and ischemic injury.

81
Q

If tissue ischemia seems similar in concept to what was described for prerenal azotemia, that is because
there is overlap. It is like the difference between

A

myocardial ischemia and a myocardial infarction.

82
Q

If there is modest hypotension or hypovolemia, BUN and creatinine will

A

rise in a 20:1 ratio consistent with prerenal azotemia. Prerenal azotemia is essentially reversible.

83
Q

If the ischemia becomes more severe, the tubular cells will

A

necrose and slough off into the urine and become visible as granular, muddy brown, or pigmented casts

84
Q

At the point of necrosis, the renal insufficiency can be ………………. In less severe disease and nonoliguric ATN, urinalysis may be relatively ………….

A

permanent

normal

85
Q

The hypotension causing tubular ischemia can be of any etiology,

A

surgical or medical. The degree, and especially the duration of hypotension, are extremely important.

86
Q

The longer the duration of hypotension/hypoperfusion, the greater the chance of ……….

A

ATN

87
Q

the likelihood of rhabdomyolysis causing renal failure is markedly increased when there is

A

hypoperfusion of the kidney.

88
Q

the likelihood of cisplatin toxicity, tumor lysis syndrome, or injury from hemoglobin toxicity causing renal failure is markedly increased when there is

A

hypoperfusion of the kidney.

89
Q

There are 3 phases in ATN, although not everyone experiences all phases

A
  • Prodromal: time between the acute injury and onset of renal failure
  • Oliguric (<400 mL/24 hrs) or anuric (<100 mL/24 hrs)
  • Postoliguric: diuretic phase when all the water not previously excreted will leave the body in a vigorous polyuria
90
Q

Diagnosis of Acute tubular necrosis

A

The initial clue is a BUN:creatinine ratio close to 10:1; by itself this ratio simply implies the damage is intrarenal (inside the kidney itself),

91
Q

Further clues to the diagnosis of ATN are

A

high urine sodium (>40), high fractional excretion of sodium (>1%), and low urine osmolality (<350)

92
Q

This is because tubular cells are responsible for forming either …………… or …………….. urine

A

concentrated or

dilute urine

93
Q

If the tubular cells die from ischemia, then the kidney can neither ……………… nor …………. the urine.

A

concentrate nor dilute the urine

Dead cells don’t work

94
Q 
Prerenal
Urine osmolarity  ..............
Urine Na+  ..............
FeNa+  ..............
Urine sediment  ..............
A

> 500
<20
<1%
Scant

95
Q 
ATN
Urine osmolarity  ..............
Urine Na+  ..............
FeNa+  ..............
Urine sediment  ..............
A

<350
>40
>1%
Full (brownish pigmented granular casts, epithelial casts may be seen)

96
Q

Treatment of Acute tubular necrosis

A

1-Treatment focuses on correcting the underlying cause
2-There is no therapy that can reverse the renal failure.
3-Hydration is often given to make sure there is no prerenal component;
4-hydration can prevent contrast-induced renal failure, but it does not reverse it once it occurs, nor can diuretics

97
Q

ATN is a combined …………../………… disease.

A

ischemic/toxic

98
Q

It is like a ‘sunburn for the kidney.’ Once it occurs, all you can do is

A

support the patient and wait to see if the renal tubular cells can restore themselves.

99
Q

If the degree of renal failure is severe and life threatening, then …………… is used.

A

dialysis

100
Q

Allergic interstitial nephritis (AIN) accounts for ………… of intrinsic renal failure

A

10–15%

101
Q

It can be distinguished from other causes of renal failure by the presence of

A

fever and rash on physical examination and many WBCs, occasionally eosinophils.

102
Q

The etiology of AIN is usually an adverse immunologic effect to

A

medication (70% of cases).

103
Q

The medications most likely to be allergenic in general are those medications most likely to cause

A

AIN

104
Q 
for example skin rash from an allergic drug reaction can be caused by
1- .............. ,
2-..............,
3-.............. , 
4-.............., 
5-.............., 
6-and ................. 
These are the same medications to cause ........... In addition, many of these same drugs cause........................... hemolysis as well.
A 
1-penicillin, 
2-cephalosporin, 
3-sulfa drugs, 
4-allopurinol, 
5-rifampin, and 
6-quinolones

AIN
drug-induced

105
Q

In other words, 10% of the population is allergic to …………….. or ……………. drugs

A

penicillins or sulfa

106
Q

This allergic reaction can take the form of a ………….., …………… …………… …………, ………….., or ……………

A

rash, Stevens-Johnson syndrome, hemolysis, or AIN

107
Q

The most common infections to result in AIN are ……………….., ………………………, ………….., ………………., and ………………….

A

leptospirosis, legionella, CMV, rickettsia, and streptococci.

108
Q 
The least common causes of AIN are several autoimmune disorders such as
1-...................
2-...................
3-...................
4-...................
A

1-systemic lupus erythematosus (SLE),
2-Sjögren syndrome,
3-sarcoidosis,
4-cryoglobulins.

109
Q

Cryoglobulins can cause renal failure from ……………..
………………… as well.

A

membranous glomerulonephritis

110
Q

clinical picture of AIN

A

1-Fever is present in 80% of those with AIN.
2-Rash is present in 25–50% of patients.
3-Joint pain is common because AIN acts somewhat like serum sickness.

111
Q

Lab abnormalities include the following:

A
  • Eosinophilia, eosinophiluria, hematuria, proteinuria, increased serum IgE
  • Hematuria (95% of patients), though this finding is rather nonspecific. More people with AIN have eosinophils in the urine rather than in the blood.
  • Mild proteinuria, nearly always <2 grams/24 hrs
112
Q

The best initial test for AIN is a ………………………… looking for white cells.

A

urinalysis (UA)

113
Q

the UA cannot distinguish …………….. from other white cells

A

eosinophils

114
Q

The most accurate test for urine eosinophils is ……………….. or ………………of the urine.

A

Hansel or Wright stain

115
Q

The most accurate test for AIN is actually …………….. ……………….., although that is not needed in the presence of the other findings above

A

kidney biopsy

116
Q

NSAID-induced injury typically lacks
1-………….,
2-………….,
3-………….

A

1-fever,
2-rash,
3-and eosinophilia

117
Q

Treatment of Allergic interstitial nephritis

A

1-There is no specific therapy necessary for AIN in most patients; it should resolve spontaneously after stopping the offending agent.
2-If renal failure persists or worsens, consider a short course of steroids.

118
Q

Rhabdomyolysis is caused by

A

sudden, severe crush injury; seizures; severe exertion; and sometimes by hypokalemia, hypophosphatemia, or medications such as statins

119
Q

Massive hemoglobinuria severe enough to cause renal failure is generally only caused by an ……………. ………………..

A

ABO incompatibility

120
Q

Both of these disorders result in enough pigment release in the bloodstream to cause ……………………

A

nephrotoxicity

121
Q

The toxicity is because the pigment is directly toxic to the ………….. …………. as well as from precipitation of the …………….. in the tubules.

A

tubular cells

pigment

122
Q

The degree of toxicity is related to the duration of

contact of the tubular cells with the ………….. or ………………

A

hemoglobin or myoglobin.

123
Q

a person who has run a marathon has both ……………… release as well as poor kidney perfusion. This is cumulative in the risk of renal failure.

A

myoglobin

124
Q

The most important test with a severe crush injury or seizure and potentially life-threatening rhabdomyolysis is an

A

EKG or potassium level

125
Q

Acidosis and hyperkalemia can lead to an ………………..

A

arrhythmia

126
Q

If there are peaked T-waves on the EKG, give ……………. …………… or ……………..

A

calcium chloride or gluconate.

127
Q

The best initial test for rhabdomyolysis is a ……….. , in which you find a dipstick positive for blood but with no red cells visible (that is because …………….. can react with the reagent on the dipstick and come out as if there were red cells present)

A

UA

myoglobin

128
Q

The dipstick of the UA cannot distinguish among …………………., …………………, and ……………
This is because myoglobin has ………….in it.

A

hemoglobin, myoglobin, and RBCs.

heme

129
Q

Rhabdomyolysis is confirmed with the following:

A
  • Markedly elevated serum CPK level (a biochemical marker of skeletal muscle neurosis)
  • Metabolic acidosis with decreased serum bicarbonate, hyperphosphatemia secondary to muscle breakdown, and hypocalcemia secondary to the deposition of calcium in damaged muscles
  • Possible severe hyperuricemia due to release of purines from damaged muscles
  • Very rapidly rising creatinine level due to the renal failure and massive release of muscle products; thus, BUN:creatinine ratio may be low (below 10:1)
130
Q

Treatment is

A

1-In general, therapy is hydration and mannitol used as a diuretic to decrease the duration of contact between the nephrotoxic hemoglobin/myoglobin and the kidney tubule.
2-Alkalinizing the urine with bicarbonate may help prevent the precipitation of the pigment in the tubule.

131
Q

If there are EKG abnormalities from the hyperkalemia, the best initial therapy is ………………… ……………… or ………………..

A

calcium chloride or gluconate.

132
Q

Bence-Jones proteins, such as in myeloma, also cause ………….. ………………..
Myeloma is most prominently a cause of ………………. ………………., however, not tubular damage

A

tubular damage

nephritic syndrome

133
Q

The most common cause of hyperoxaluria resulting in acute renal failure is …………….. ……………… ………………. in a suicidal person who ingests ……………….. Look for an intoxicated person with metabolic acidosis and elevated anion gap who is found to have renal insufficiency. Diagnosis is confirmed with …………… …………….. seen on urinalysis.

A

ethylene glycol overdose
antifreeze.
oxalate crystals

134
Q

Look for an intoxicated person with metabolic acidosis and elevated anion gap who is found to have renal insufficiency.
Diagnosis is confirmed with

A

oxalate crystals seen on urinalysis

135
Q

Treat acute ethylene glycol overdose with ……………… ……………… to prevent the formation of the toxic metabolite of ethylene glycol,

A

fomepizole infusion

136
Q

Dialysis must also be used to then remove the …………… ……………….. Sodium bicarbonate can be given to correct …………….

A

ethylene glycol

acidosis

137
Q

Chronic hyperoxaluria and kidney stones can be caused by ………………… ……………….. because of fat and calcium malabsorption.

A

Crohn’s disease

138
Q

Acute renal failure from uric acid toxicity occurs in the setting of ………………. ……………….. …………. . This is why patients with ………………. or …………………. receive vigorous hydration and allopurinol prior to receiving chemotherapy.

A

tumor lysis syndrome

leukemia or lymphoma

139
Q

…………………..reduces the production of uric acid by inhibiting conversion of xanthine to hypoxanthine to uric acid

A

Allopurinol

140
Q

Uric acid stones precipitate in an…………… ……………. , unlike oxalate crystals, which precipitate in ……………. …………….

A

acidic urine

alkaline urine

141
Q

Allopurinol treatment with ………………. of urine markedly reduces the risk of uric acid nephropathy

A

alkalinization

142
Q

Chronically, …………. causes renal impairment through a slower and milder version of the same mechanism.

A

gout

143
Q

In hypercalcemia, calcium precipitates in the kidney tubule, forming ………….

A

stones

144
Q

The most common cause of hypercalcemia is ……………… ………………………

A

primary hyperparathyroidism

145
Q

If there is no renal damage (or decreased GFR) and no symptoms, i.e., mild hyperparathyroidism.
treatment is …………….. ……………
If the hyperparathyroidism is associated with evidence of renal impairment, treatment is ……………. ……………… …………………..

A

not surgical

surgical resection of the glands.

146
Q

The most common toxins to be associated with renal insufficiency and ATN are

A

NSAIDs; aminoglycosides; cephalosporins;
contrast agents; amphotericin;
chemotherapy e.g., cisplatin;
radiation effect;
heavy metals e.g., lead, mercury, gold; and cyclosporine.

147
Q

1-Allergic interstitial nephritis occurs with the ………. …………. , and is associated with ………. , ………. , ………. ………. , and ………. in both blood and urine.

A

first dose

fever, rash, joint pain, and eosinophils

148
Q

Direct-acting toxins can take days to weeks to produce enough cumulative toxicity to cause ………. ……….; they are not associated with eosinophils, fever, joint pains, or rash

A

renal failure

149
Q

There is no test which can confirm a specific toxin as the etiology of the renal failure. Other causes of renal failure must first be ……………. , and the toxin must be found in the history.
Regarding treatment, there is no ……………. ………… that can reverse the renal insufficiency of any direct-acting toxin.

A

excluded

specific therapy

150
Q

………………… toxicity generally takes 5–10 days of administration to result in toxicity

A

Aminoglycoside

151
Q

Renal failure due to aminoglycosides is

A

non-oliguric (K+ levels not elevated)

152
Q

Hypokalemia and hypomagnesemia predispose

the patient to

A

aminoglycoside toxicity

153
Q

The ability of antibiotics to kill bacteria is associated with the peak level, but the likelihood of toxicity is associated with the …………………

A

trough level

154
Q

This is most because a low trough allows time for the renal tubular cells and neural cells of the inner ear to

A

regenerate themselves.

155
Q

Aminoglycosides also exert a bactericidal effect after their level has become low because they enter the bacteria and continue to kill. This ability to exert an effect despite low or absent levels is called

A

postantibiotic effect

156
Q

Once-a-day dosing allows high bactericidal levels with the same efficacy and very low trough levels. The low trough levels …………….. ……………..

A

reduce toxicity

157
Q

Aminoglycoside-related nephrotoxicity is estimated to be between 10–20% of all ………………………………………… and is usually reversible

A

drug-induced nephrotoxicity

158
Q

Amphotericin B associated with

A

renal insufficiency and distal renal tubular acidosis.

159
Q

These often revert to normal after the medication is stopped. This form of toxicity is …………….. ……………….

A

cumulative dosing

160
Q

It is expected that after several days or weeks of amphotericin use, the patient will develop

A

a high creatinine as well as a decreased magnesium, bicarbonate, and potassium
level.

161
Q

clinical picture of Atheroembolic Disease.

A

Look for a patient who undergoes a vascular catheter procedure such as angioplasty who develops renal failure several days later

162
Q

the most accurate test is a …………… …………. to see cholesterol crystals in the skin, this is rarely done.

A

skin biopsy

163
Q

ttt of Atheroembolic Disease.

A

There is no therapy for atheroemboli. High doses of statins have been tried.

164
Q

Radiocontrast material for CT scanning can result in renal failure in as little as …………… hours after the use of the agent. This is one of the main ways to distinguish this form of renal failure from aminoglycoside or amphotericin toxicity, which need …………………………………….. of cumulative exposure.

A

12–24

several days to weeks

165
Q

The rise in creatinine peaks at………….. days after the injury.
The BUN and creatinine may be up in a ……….. ratio, such as in prerenal azotemia, because the hypertonicity of the agent provokes an intense vasospasm of the …………….. …………….

A

3–5
20:1
afferent arteriole

166
Q

The worse the underlying ……………………………., the more likely the patient is to have renal failure secondary to contrast material.

A

renal parenchyma

167
Q

If you are elderly, diabetic, and hypertensive with myeloma, you are far more likely to experience

A

contrast-induced renal insufficiency

168
Q

………………. is associated with renal failure in addition to its toxicity on the pancreas.

A

Pentamidine

169
Q

Vancomycin, cyclosporine, and lithium can all cause renal failure in a ……………………………………….

A

dose-dependent fashion

170
Q

………………….. is a protease inhibitor that results in renal failure usually from the drug precipitating out in the kidney tubules

A

Indinavir

171
Q

NSAIDs are a frequent cause of renal failure. NSAIDS cause renal failure by several mechanisms:

A 
1-Interstitial nephritis
2-Direct toxic effect on the tubules
3-Papillary necrosis
4-Inhibition of vasodilatory prostaglandins in the afferent arteriole
5-Membranous glomerulonephritis
172
Q

A person without underlying renal insufficiency should not experience a rise in

A

creatinine

from the use of NSAIDs

173
Q

That only occurs in those with significant impairment such as the

A

1-elderly or
2-with hypertension
3-or diabetes

174
Q

NSAIDs can also cause …………… by a combination

of these.

A

toxicity

175
Q

More than 50% of patients have pyuria, which, if persistently associated with sterile urine, can be an important clue to

A

diagnosis.

176
Q

There is no specific test to confirm that NSAIDs caused .

A

the renal failure

177
Q

There will be a rise in

A

BUN and creatinine and a history of NSAID use

178
Q

There is no specific therapy other than to stop the

A

NSAID.

179
Q

Acute papillary necrosis occurs in patients with a history of

A

1-sickle cell disease,
2-diabetes,
3-urinary obstruction,
4-chronic pyelonephritis.

180
Q

It can be brought on acutely by the ingestion of

A

NSAIDs

181
Q

The presentation of Acute papillary necrosis is

A

1-the sudden onset of flank pain,
2-hematuria,
3-pyuria,
4-and fever.

182
Q

This can be very similar in presentation to

A

acute pyelonephritis.

183
Q

In a patient with the risks described, symptoms for ……………. ………………… will come on very suddenly

A

papillary necrosis

184
Q

The findings of ……………. and ………………… on urinalysis will not distinguish them. However, papillary necrosis will not grow any organisms on culture. The most accurate diagnostic test for papillary necrosis is …………., which will show ………….. contours in the renal pelvis where the papillae have sloughed off. There is no specific therapy for papillary necrosis.

A

white and red cells
CT scan
“bumpy”

185
Q

In patients with significant underlying renal disease who require a radiologic procedure requiring contrast, what is is required before the procedure.

A

hydration with 1–2 liters of normal saline over 12 hours

186
Q

Prevention of contrast-induced renal failure

A

1-Hydration has been shown to decrease the likelihood of contrast-induced renal failure.
2-Bicarbonate and N-acetyl cysteine have been shown to decrease the risk of renal failure.
3-Ineffective preventive measures are diuretics such as furosemide or mannitol.

Nephrology (5 decks)

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