Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Renal > Differentiating Pre-renal, Intrinsic Renal and Post-renal disease > Flashcards

Differentiating Pre-renal, Intrinsic Renal and Post-renal disease Flashcards

1
Q

How can a urinary obstruction cause chronic kidney disease and even ESRD?

A

Obstruction causes fluid to back up increasing pressure. This pressure in the tubule decreases GFR causing intrarenal vasoconstriction which leads to:

  1. ischemic tubular injury
  2. interstitial fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What assessment is most helpful in determining post-renal obstruction?
What is the exception?

A

sonography

CT imaging in the case of retroperitoneal fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What assessments are most useful for determining pre-renal disease?

A
  1. BUN/Cr ratio is elevated
  2. hematocrit
  3. urinary Na
  4. BP and pulse
  5. albumin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why are diabetics more prone to post renal obstruction?

A

They have neurogenic bladder which is more prone to stasis –> infection, stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

When would you suspect retroperitoneal fibrosis in a patient?

A

It they have acute kidney injury, flank pain/abdominal pain where pre-renal and kidney disease are excluded.

Especially in patients with lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is type IV RTA?

A

hyperkalemia renal tubular acidosis.
The CCD does not secrete acid or K into the urine because the obstruction separates the PC and IC which dissipates the lumen negative potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the cardinal feature of pre-renal azotemia?

A

decreased EABV

  1. history of fluid loss, decreased fluid intake
  2. postural hypotension
  3. CHF edema
  4. cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does pre-renal azotemia cause acute/chronic renal disease?

A

Pre-renal azotemia has decreased EABV which increases the release of AII and sympathetic nerves which cause renal vasoconstriction.
This can reduce RBF and GFR.
Aldosterone AND ADH are activated to conserve Na and water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do you differentiate pre-renal disease from acute tubular necrosis?

  1. Una
    2.Ucl
    3FEna
  2. U/P creatinine
  3. U/P urea
  4. Uosm
  5. sediment
A

Pre-renal:

  1. low
  2. low
  3. less than 1%
  4. over 40
  5. over 40
  6. concentrated
  7. normal, hyaline cast

Post-renal:

  1. high
  2. high
  3. > 2%
  4. over 20
  5. over 20
  6. iso-osmolar
  7. granular, cellular casts (muddy brown)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

If you have a low volume state, what happens to the filtration fraction?

A

The GFR increases because there is decreased tubular hydrostatic pressure and increased peritubular oncotic pressure.
The RBF is decreased because volume is decreased.
This leads to an increased FF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

in pre-renal states, what happens to the urinary sodium and the urinary concentration?

A

There is reduced Na in the urine because low volume–> AII–> aldo–> reasorbs Na distally and AII–> increased proximal Na resorption

Urinary Na decreases and urinary concentration increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are 3 situations where urinary Na and Cl are high?

A
  1. diuretics
  2. adrenal insufficiency
  3. renal Na waste (liddle, barter, gitelman)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are 4 situations of where urinary Na is high and urinary Cl is low?

A
  1. NRA
  2. bicarbonaturia
  3. ketoacids
  4. penicillin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the only situation with low urinary Na and high urinary Cl?

A

Increased Unh4V (chronic diarrhea)

Increased na+k-cl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why does vomiting cause hyponatremia?

A

The vomiting depletes volume and makes the person metabolically alkalotic.
The HCO3 acts as a NRA which pulls out Na in the urine.
The volume depletion with the vomiting increases ADH which retains water.
This makes the body hyponatremic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

When a person is vomiting, what happens to the BUN and Cr?

A

BUN and Cr are both elevated in the plasma, but BUN/Cr is increased at a rate of 20:1.
This is because the proximal reabsorption of urea is increased (in the same way that Na is)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

In addition to hyponatremia, what serum electrolyte abnormalities are associated with vomiting?

A
  1. hypokalemia- due to low EABV and increased Na reabsorption in the CCD because HCO3 is a NRA
  2. hypochloremia because the loss of Cl in vomiting and the dilution due to increased free water
  3. Total CO2 is elevated due to the loss of HCl and is maintained by the low volume and hypokalemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does urinalysis associated with vomiting show for Na and Cl levels?

A

Na and Cl are decreased in the urine because of avid tubular reabsorption. Urine Na> Cl because it is dragged out with HCO3

19
Q

How can you determine the urine osmolarity from the specific gravity?
What are situations when this does not work?

A

Take the specific gravity and multiply the last digits by 35.
1.020 = 20x35 = 700

This does not work with proteinuria or glycosuria

20
Q

What are the 2 usual causes of acute tubular necrosis?

A
  1. hypoxia

2. nephrotoxic agents

21
Q

What are the 3 causes of hypoxia that can lead to ATN?

A
  1. shock
  2. sepsis
  3. hemorrhage
22
Q

What are the common nephrotoxic injuries that can cause ATN?

A
  1. aminoglycosides
  2. myoglobin
  3. radiocontrast
  4. antibiotics
23
Q

What 3 things lead to the reduction of GFR and onset of azotemia in a person with ATN?

A
  1. The cell death leads to sloughing and tubular obstruction.
  2. The loss of tubular integrity leads to backleak of solutes
  3. Renal vasoconstriction also occurs.

These 3 things lead to decreased GFR and azotemia

24
Q

What is the effect of ATN on volume?

A

Because GFR is decreased salt and water intake exceed the kidneys ability to excrete.
This leads to volume overload.

25
Q

ATN can be oliguric or non-oliguric. What is the difference?

Which is more severe?

A

Oliguric= when urine flow is less that 400ml/day.
This is more severe because it is complicated by greater azotemia and volume overload.

Non-oliguric = urine flow is more than 400ml/day. It is less severe and occurs with mild ischemia or after the administration of toxins (radiocontrast, aminoglycosides. It does not have volume overload or hyperkalemia.

26
Q

What is the only electrolyte that falls in the serum when oliguric acute tubular necrosis occurs?

A

Ca because the serum phosphorus increases and binds it.

Also, there is a decrease in 1,25 vit D so less Ca will be absorbed from the intestines

27
Q

What is the initial sign of recovery from ATN?

A

Increase in urine flow.

The BUN and Cr continue to rise, then plateau, and then fall. It takes 4-5 days to fully recover

28
Q

With ATN the serum Na and Cl will be _________ while K will be __________.
What acid/base disorder do these patients usually present with?

A

Na and Cl are low and K is high.
The patient presents with metabolic acidosis with increased anion gap.
The BUN/Cr ratio however is still 10/1

29
Q

Why does ATN cause metabolic acidosis?

A

The tubules of the kidney are crucial for the recapturing and regeneration of HCO3, so if the tubules are necrosed, they will not be able to replenish HCO3

30
Q

What are the 2 most important underlying factors for the development of ATN from radiocontrast (contrast neuropathy)?

A
  1. CKD

2. diabetes

31
Q

When someone has a crush injury, what are the 2 ways the kidney gets messed up?
When should rhabdomyolysis be considered?

A

Rhabdomyolysis develops with muscle injury which leads to the release of myoglobin.

Myoglobin:

  1. is directly toxic to the renal tubule cells
  2. causes intratubular obstruction

Consider rhabdo if serum creatinine kinase >5000 U/L with heme positivity on urine dipstick

32
Q

When do NSAIDs cause ATN?

A

In volume depleted states because the low volume will increase AII, catechols, ADH, sympathetic nerves which leads to vasoconstriction to maintain systemic BP.

The kidney normally protects from too much vasoconstriction by releasing PGs. This decreases RBF to maintain function. If PGs are blocked (NSAIDS) there will be too much vasoconstriction

33
Q

What is the primary source of renal emboli?

A
  1. Mural thrombi common in patients with atrial arrythmia or prior MI
  2. bacterial endocarditis
34
Q

What gross finding would be consistent with a renal emboli?

A

A wedge shaped infarct radiating out from the affected vessel

35
Q

How long does it take to establish irreversible necrosis in the kidney?

A

If the artery is occluded 2 hours or longer

36
Q

What physical exam findings would be consistent with renal emboli?

A
  1. skin lesions
  2. focal neurological deficits
  3. flank pain/abdominal tenderness
  4. BP rise as a result of RAAS
37
Q

What laboratory finding is “highly suggestive” of renal infarction?

A

elevated serum lactate dehydrogenase (5x greater than normal) with little or no elevated serum transaminase

38
Q

What is the diagnostic test of choice for suspected renal emboli?

A

Radioisotope renogram- demonstrates segmental/generalized lack of perfusion.

39
Q

What is cholesterol crystal embolization?
When does it usually occur?
What extra-renal sites can these emboli go to?

A

It is a cause of AKI in patients with diffuse atherosclerotic disease.
It generally occurs after coronary angiography or aortic surgery.
1. livedo reticularis (skin)
2. retinal artery (Hollenhorst plaque)

40
Q

Who is most likely to develop renal venous thrombosis?

What is the only clinical clue to the presence of RVT?

What is the gold standard for diagnosis of RVT?
What is the most common and non-invasive test?

A

A patient with nephrotic syndrome (membranous GN) is at increased risk because they have decreased fluid loss across the glomerulus and will have hemoconcentrated blood in the veins making them hypercoagulable.

A pulmonary embolism is the only clinical clue to the presence of renal or other DVT.

Gold standard ; inferior vena cavagram with renal venography, spiral CT, MRI

Most common/non-invasive: MRI

41
Q

If there is significant (>70%) bilateral renal artery obstruction or PKD pressing on the renal artery, how does the body adapt to maintain intraglomerular pressure?

A

JG cells sense low flow–> Renin–> AI–>AII–> constricts efferent vessel

42
Q

If a patient is volume constricted, why would you hold the ACEI/ARB until the ECFV is replenished?

A

In a low volume state, you want AII to constrict the efferent arteriole to maintain GFR.
ACEI would block this effect

43
Q

What 2 anatomical and 3 functional situations would an ACEI be avoided?

A
  1. Renal artery stenosis
  2. PCKD
  3. decreased EABV
  4. NSAIDs, cyclosporin A
  5. sepsis

Renal (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions