AKI Flashcards

1
Q

What is AKI

A

It’s acute/ abrupt decline in kidney function leading to increased serum creatinine or decreased urine output or both

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

How quickly does AKI develop?

A

Over hours to days with progressive elevated BUN creatinine and potassium with or without oligouria

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

What is Azotemia?

A

Elevation of serum creatinine and BUN related to inability of renal system to filter waste

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

What is uraemia ?

A

Decrease of n renal function to point where symptoms begin to develop in multiple body systems
Elevated BUN and Cr causes anorexia, vomiting, purities, or itchiness and neurological changes
Manifestations due to accumulation of waste products in blood and electrolytes imbalance and inflammation

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

Oligouria

A

Urine output less than 30ml/hr or less
Or less than 400ml/day

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

What are the 3 categories of AKI?

A

Pre-renal
Intra-renal
Post renal

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

Pre- renal AKI is what

A

Decreased renal perfusion and filteration

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

What is pre-renal AKI related to?

A

It’s related to factors that reduces renal blood flow leading to decreased glomerular perfusion and filtration

Hypovolemia, decreased cardiac output as well as vascular obstruction can cause pre-renal AKI

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

How do the body auto compensate if perfusion is low

A

With Decrease circulatory volume auto regulatory mechanisms that increase angiotensin II, aldosterone, norepinephrine and anti diuretic hormones (ADH) to try to preserve blood flow to essential organ

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

Pre-renal Azotemia is associated with what?

A

Decrease excretion of sodium
Increased salt and water retention
Decreased urine output

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

What are the causes of AKI

A

Vasoactive meds- ACE-I, ARBs, epinephrine, dopamine
NSAIDs
Radioconstrast agents

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

What’s the mode of action of medication that cause AKI?

A

The vasoconstriction meds- ACE-I, ARBs, epinephrine, dopamine
NSAIDs and radiocontrast agents cause renal vasoconstriction leading to hypoperfusion of the glomeruli

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

True or false?
AKI associated with pre-renal is reversible

A

True

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

Intra- renal causes of AKI

A

Glumerulonephritis
Vascular causes- renal vein thrombosis or renal infraction
Interstitial disease

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

What is nephrotic syndrome

A

Sequela of glumeronepritis

Expression of 3.5g or more protein in urine per day

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

Acute tubular necrosis is due to what?

A

Ischemia- disruption of glomerular base membrane and patchy destruction of tubular epithelium
Nephrotoxin: necrosis of tubular epithelium cells which slough off and plug renal tubules

17
Q

Pathophyology of acute tubular necrosis

A

Hypovolemia & decrease renal blood flow
Activate RAAS resulting in constriction of peripherial arteries and renal after ent arteioles
Decreased blood flow = decrease glumerullar capillary pressure and decreased GFR and tubular dysfunction contributing to oliguria
Ischemia = decrease permeability of glumerular cells
Damaged nephron leads to development of edema and collection of necrotic cells
Necrotic cells decrease glumerular filtration and increase pressure within the tubules
Glumerular leak blood
Decrease fluid flow within the tubules
Ultimately leads to oliguria

18
Q

Under what condition is acute tubular necrosis reversible

A

If Ischemia is not prolonged
Basement membrane is not destroyed
Tubular epithelium regenerate

19
Q

What are the causes of post renal AKI?

A

Obstruction of urine flow
Back up of urine into renal pelvis which impairs kidney function

20
Q

Most common cause for d Post renal causes of AKI

A

Prostatic hyperplasia
Prostate cancer
Renal calculi
Trauma
Extrarenal turmors

21
Q

Post renal cause of AKI account to what percentage

A

5%

Post renal AKI is almost always treatable if identified before permanent kidney damage

22
Q

What are the 4 stages of AKI

A

Initiation phase
Extension phase
Maintenance phase
Recovery phase

If patient does not recover, they develop CKD

23
Q

What’s the xtics of initiation phase

A

Increased serum creatinine
Increase BUN
Decrease urine output

24
Q

Extension phase

A

Progressive Ischemia
Inflammation

25
Q

Maintaince phase

A

Decreased urine output, body unable to excrete waste
Can last days to weeks
10-14days usually
May last month- longer duration = poorer prognosis
Xtrised by changes in urine output, fluid and electrolyte abnormalities and uremia

26
Q

What’s the most common cause of AKI in hospitalized patients

A

Sepsis. It cause’s hypotension