Acute Kidney Injury Flashcards

1
Q

Define AKI.

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

What are the RFs for developing an AKI?

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

What are the pre-renal causes of AKI?

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

What are the symptoms of a pre-renal AKI?

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

What are the intra-renal causes of AKI?

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

What are the symptoms of an intra-renal AKI?

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

What are the symptoms of uraemia?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the possible causes of a rash in the presence of a decreased urine output?

A

AIN type 1 = autoimmune causes => SLE, sjogrens, IgA Nephropathy, vasculitis
Type 2 = drug induced => NDAP

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

Describe the pathogenesis of glomerulonephritis including its clinical effects.

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the two main causes of ATN?

A

Ischaemia and nephrotoxins.

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

What are key investigations for ATN?

A

(urine analysis) + for casts

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

What would you expect to see on urine analysis in ATN?

A

A urinalysis of Acute Tubular Necrosis (ATN) typically shows the following key findings:

Microscopic Examination:

Muddy Brown Casts: Granular casts made of degenerated tubular epithelial cells and proteins; a hallmark of ATN.

Epithelial Cell Casts: Shed tubular cells clumped together; also highly suggestive of ATN.

Tubular Epithelial Cells: Free tubular epithelial cells may also be visible in the urine.

Chemical Analysis:

Low Urine Specific Gravity (<1.015): Indicates the kidney’s inability to concentrate urine due to tubular damage.

Low Urine Osmolality (<350 mOsm/kg): Poor tubular reabsorption capacity.

High Urine Sodium (>40 mmol/L): Reflects impaired sodium reabsorption in damaged tubules.

Fractional Excretion of Sodium (FENa >2%):
Helps differentiate ATN from prerenal azotemia.
In ATN, damaged tubules cannot retain sodium efficiently.

BUN/Creatinine Ratio (<20:1):
Suggests intrinsic renal damage rather than prerenal causes of AKI.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How would you differentiate between pre-renal AKI and ATN?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What triggers AIN?

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

What are the types of AIN and what are the features of each?

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

What are the post-renal causes of AKI? Include symptoms.

A
17
Q

What are ALL the causes of AKI?

A
18
Q

What are ALL the causes of AKI? Include symptoms

A
19
Q

What would you expect on general and closer inspection of an AKI case?

A
20
Q

What would you expect on palpation, percussion and auscultation of an AKI case?

A
21
Q

What special tests would you offer for an AKI case? (physical exam)

A
22
Q

What are all the exam findings of AKI?

A
23
Q

How would you grade AKI?

A
24
Q

What are all the investigations for an AKI?

A
25
Q

What are all the investigations for AKI, including those exclusive to CKD?

A
26
Q

What ECG changes would you expect in hyperkalemia?

A
27
Q

What is the management of hyperkalemia?

A

DO NOT USE HARTMANN’S!!

28
Q

What is the conservative management of an AKI?

A
29
Q

What is the full management of an AKI?

A
30
Q

List the complications of an AKI.

A