Acute kidney injury lo's Flashcards
1
Q
Acute kidney injury
A
Rapid decrease in glomerular filtration that results in abnormal fluid and electrolytes balance and azotemia, increase in serum creatinine abruptly
2
Q
Cause of acute kidney injury
A
- pre-renal
- intrinsic
- post-renal
3
Q
Pre-renal (60%)
A
- conditions that cause reduced renal perfusion
- hypovolemia (vomiting, diarrhea, sweating, burns, diuretics, dehydration)
- Hypotension (sepsis, cardiogenic shock –> decreased CO, anaphylactic shock
- Decreased circulating volume eg congestive heart failur, cirrhosis, liver failure, abdominal compartment syndrome, nephrotic syndrome, acute pancreatitis
- Renal artery stenosis
- Drugs ( NSAID’s, ACE inhibitors, cyclosporine, tacrolimus)
4
Q
renal/intrinsic AKI (35%)
A
- Any condition that leads to severe direct kidney damage
- Acute tubular necrosis (85%)
- Acute interstitial nephritis
- Vascular diseases
- Glomerulonephritis
5
Q
Post-renal (5%)
A
- any condition that results in bilateral obstruction of urinary flow from the renal pelvis to the urethra
- benign prostatic hyperplasia
- tumors (bladder, prostate, cervical, metastases)
- stones
- neurogenic bladder
- congenital malformations (posterior urethral valves)
- Iatrogenic (catheter-associated injuries)
6
Q
Azotemia
A
- elevation or buildup of nitrogenous products in the blood (BUN)
7
Q
Creatinine
A
waste product from wear and tear of muscles
8
Q
Do patients with unilateral urethral obstruction maintain normal serum creatinine levels?
A
Yes as long as contralateral kidney remains intact
9
Q
Acute tubular necrosis and causes
A
- damage and death of epithelial cells that line tubules
- Ischemia due to prolonged hypotension
- Nephrotoxic drugs eg radiographic contrast agents, aminoglycosides, methotrexate, amphotericin B
- Endogenous toxins eg bence jones protein light chains in MM
10
Q
glomerulonephritis and causes
A
- inflammation of glomeruli
- Bacterial endocarditis, HIV, HepB/C, post-streptococcal glomerulonephritis
11
Q
Acute interstitial nephritis and causes
A
- inflammation of renal interstitium
- Medication eg antibiotics, phenytoin, interferon, PPI’s, NSAID’s, cyclosporin
- Infection eg candida, legionella spp, streptococcus spp, hepatits C, sarcoidosis, amyloidosis
12
Q
principal laboratory findings that indicate acute kidney injury
A
- Urea: increased
- Creatinine: serum creatinine will increase
- Sodium: hyponatemia? due to water overload
- Potassium: hyperkalemia
- Calcium: hypocalcemia due to decreased production of of 1,25 OH vitamin d
- Phosphate: hyperphosphataemia, unable to excrete phosphate
- Bicarbonate: metabolic acidosis
- decrease in urine output
- Normocytic anemia
13
Q
Pathology of acute tubular necrosis
A
- necrotic proximal tubular cells fall into tubular lumen –> debris obstructs tubules–> decreased GFR –> activation of RAAS–> increased aldosterone release–> increased reabsorption of Na+, H2O–> increased urine osmolality –> ADH secreted –> increased reabsorption of H20/urea
14
Q
cytological and histological findings of acute tubular necrosis
A
- muddy brown granular casts
- epithelial cell casts
- free renal tubular epithelial cells ( due to denudation of the tubular basement membrane)
15
Q
Management pre-renal failure
A
- correct pre-renal factors
- correct volume overload
16
Q
Management intrinsic renal failure
A
- Consider trial of IV fluids; identify and treat underlying causes that require specific interventions
- discontinue nephrotoxic drugs, treat infection
17
Q
Management post-renal failure
A
- Relieve the urinary tract obstruction
- stenting, catheter
18
Q
Phase of AKI
A
- onset/initiation: blood flow to kidneys decreases and urine output decreases, hours to days
- Oliguric: Urine output less than 400ml/day. Kidneys stop functioning properly, 1-2 weeks, increases in creatinine and urea
- Diuretic: will happen if damage has stopped and kidneys get more blood flow. Diuresis between 4-5l per day. 1-2 weeks
- Recovery: urine output and GFR normalizes. Months to yeas
19
Q
Causes acute tubular necrosis
A
- Toxic: injury occurs directly due to nephrotoxic substances
- Ischemic: injury occurs secondary to decreased blood flow
20
Q
Indications for initiation of artificial renal support (dialysis)
A
- Refractory fluid overload
- Electrolyte imbalances
- Acid-base disturbances
- Acute poisoning
- Uremic symptoms
21
Q
Advice for patients with AKI on discharge
A
- Avoid nephrotoxic medications and drugs that may have a detrimental effect on glomerular perfusion
- Ensure adequate protein and calories intake
- Educate patients on medication and diet
22
Q
Pathophysiology of pre-renal AKI
A
- Decreased blood supply to kidneys (due to hypovolemia, hypotension or renal vasoconstriction) –> failure of renal vascular autoregulation to maintain renal perfusion–> decreased GFR–> activation of renin-angiotensin system–> increased aldosterone release–> increased reabsorption of Na+, H2O–> increased urine osmolality –> secretion of ADH–> increased reabsorption of H20 and urea
- creatinine is still secreted in the proximal tubules so blood BUN: creatinine ratio increases
23
Q
Pathophysiology of intrinsic AKI
A
- damage to vascular or tubular component of the nephron–> necrosis or apoptosis of tubular cells–> decreased reabsorption capacity of electrolytes, water and/or urea (depending on location of injury along tubular system)–> increased Na+ and H2O in urine–> decreased urine osmolality
24
Q
Pathophysiology of post-renal AKI
A
- bilateral urinary outflow obstruction (eg stones, BPH, neoplasia, congenital abnormalities)–> increased retrograde hydrostatic pressure within renal tubules–> decreased GFR and compression of renal vasculature–> acidosis, fluid overload and increased BUN, Na+ and K+
- normal GFR can be maintained as long as one kidney functions normally
25
Q
Oliguria
A
- reduced urine output
26
Q
Anuria
A
- absence of urine output
