AKI - Acute Kidney Injury Flashcards

1
Q

What is the best method of assessing kidney function. What is the normal range

A

GFR or eGFR: Normal = 100-120

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2
Q

State the causes of Pre-renal AKI (10)

A

Reduced blood flow
Absolute: Diarrhea, vomiting, severe burns, major hemorrhage, dehydration
Relative: Distributive shock (sepsis), Adrenal insufficiency, CCF, ACE inhibitors, renal artery stenosis, embolus

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3
Q

What is azotemia?

A

increased nitrogen products in the blood => increased urea

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4
Q

What is the normal urine output range?
What is considered reduced or oliguria?
What is considered severe?

A

Normal = 0.5-2ml/kg/hr
Oliguria = <0.5ml/kg/hr
Severe <0.3ml/kg/hr

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5
Q

Define AKI

A

reduced renal function leading to increased serum creatinine and/or reduced urine output (<0.5ml/kg/hr)

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6
Q

Urea may deposit in the skin causing skin discoloration. What color is it? In severe uremia what does it become?

A

Grey-yellow colour
Severe = Uremic frost (white flakes)

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7
Q

State the signs and symptoms of uremia

A

Nausea, dizziness, anorexia
Encephalopathy: Asterixes, confusion, disturbed sleep
Pruritis with scratch marks
Skin discoloration (grey-yellow discoloration)
Pericarditis - Pericardial rub

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8
Q

Uremia may eventually lead to pericarditis. What finding would support this? Describe the finding

A

Pericardial rub. scratchy creaky sounds like rubbing leather.
Heard loudest over left sternal border (2-3 intercostal space)

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9
Q

Rash in the setting of oliguria. What are your differentials

A

HUS - hemolytic uremic syndrome
HSP (IgA vasculitis)
SLE
Sepsis

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10
Q

What are the risk factors for an AKI?

A

5 on your HANDS Mneumonic
Hypertension
Age
Nephrotoxins - Aminoglycosides, heavy metals (Lead), ethylene glycol, myoglobin (increased CPK in rhabdomyolysis), uric acid (tumor lysis syndrome), tetracycline, IV contrast, ACE inhibitors
Diabetes
Systolic BP<90 (hypotension)

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11
Q

What is tumor lysis syndrome and with relation to the kidney what may it cause?
What other acute condition may it cause? How is it treated?

A

Tumor lysis syndrome is caused by the quick turnover of cells typically occurring in chemotherapy. This leads to the release of high amounts of uric acid leading to Acute tubular necrosis.

High serum uric acid levels may also cause gout. This is treated acutely with Colchicine + hydration and chronically (preventative) with Allopurinol + hydration

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12
Q

Give 5 causes of intra-renal AKI

A

Acute Tubular Necrosis
Glomerulonephritis
Acute interstitial nephritis
Hepatorenal syndrome
HUS - Hemolytic uremic syndrome
TTP - Thrombotic Thrombocytopenic Purpura

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13
Q

How would you differentiate between a Pre-renal cause and Acute Tubular Necrosis?

A

We use serum BUN and urinalysis with sedimentation examination
Pre-renal vs ATN
BUN or urea creatinine ratio in serum: >20:1 vs Normal or <15
FeNA: <1% vs >2%
Urine Na: <20 vs >35 mEq/L
Urine osmolality: >500 vs <350 mosm/kg
Casts: None vs Brown, muddy cell casts (epithelia)

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14
Q

Acute Tubular Necrosis:
What are the causes?
Explain the pathophysiology

A

Causes:
Ischemia => any pre-renal cause
Nephrotoxins => Aminoglycosides, heavy metals (lead), myoglobin, Uric acid, Ethylene glycol

Pathophysiology:
Dead tubular cells (from ischemia or nephrotoxins) slough off and plug the tubule causing an obstruction which can produce brown cellular casts in urine. This leads to increased tubular pressure causing:
reduced GFR => Oliguria and Azotemia
reduced gradient of diffusion => Hyperkalemia and metabolic acidosis
Intrarenal damage => reduced reabsorption => increased elimination of Na, urea, and water

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15
Q

Explain the pathophysiology of glomerulonephritis in the context of AKI

How would you SCREEN for GN?

A

Antibody deposition leads to the activation of the complement system (C3/C4) which recruits macrophages to attack the podocytes leading to increased permeability => Hematuria (micro) and Proteinura (<3.5g/day). This leads to
hypoalbuminemia => Oedema and HTN
reduced gradient => reduced GFR => Oliguria and azotemia

C3/C4, electrophoresis, ASOT

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16
Q

What organism may cause Struvite stones?

A

Proteus

17
Q

Where does oedema typically begin?

A

Peripheries and facial swelling

18
Q

Type 1 hypersensitivity will recruit which type of cells?

A

Eosinophils

19
Q

Type 4 hypersensitivity will recruit which type of cells?

A

Neutrophils

20
Q

What immunoglobulin is associated with eosinophilia?

A

IgE

21
Q

What are your differentials for flank pain (and hematuria by default)?

A

UTI
Pyelonephritis
Kidney stones
Renal papillary necrosis
Acute interstitial nephritis

22
Q

What is Renal papillary necrosis?
What is it caused by (3)?
What does it present with?

A

It is the ischemia of papillae of the collecting ducts which transport urine to the calyces and into the ureters
Causes: Late interstitial necrosis, chronic analgesic use, diabetes, pyelonephritis, sickle cell disease
Presents with hematuria and flank pain

23
Q

Give the causes of Acute interstitial Nephritis
Explain the pathophysiology of Acute Interstitial nephritis

A

This is caused by a hypersensitivity reaction to penicillin, NSAIDs and Diuretics
It is a Type 1 and 4 hypersensitivity reaction leading to the recruitment of eosinophils and neutrophils respectively leading to eosinphilia, rash (IgE), oliguria
If the medications aren’t stopped, it may lead to Renal Papillary necrosis which may present with Hematuria and Flank pain

24
Q

Give 5 causes of Post-renal AKI
What is the main mechanism of kidney injury in these cases?

A

Compression: Intraabdominal tumours, prosatatic hyperplasia, prostatitis, prostate carcinoma
Blockage: Kidney stones, Struvite stones (proteus), blocked catheter
Neurogenic bladder

Main cause = obstruction leading to hydronephrosis. This mimics pre-renal early on (as obstruction) and intrarenal after (as it has caused damage to the renal cells)

25
Q

increased serum myoglobin is a cause of ATN. What disease may lead to this? What is the main investigation to confirm this?

A

Rhabdomyolysis which causes muscle injury leading to increased CK (this is the test) and myoglobin.

26
Q

What imaging would you conduct for a patient with AKI?

A

Renal Ultrasound and CXR

27
Q

What findings would you be looking for in AKI with renal US?

A

Hydronephrosis, ureter obstruction, hyperechoic in pyelonephritis (gas)

28
Q

Pulmonary oedema may occur in a range of diseases including AKI, CKD, and CCF. What imaging would you use to confirm this? and what findings would you be looking for?

A

CXR: ABCDE Mneumonic
Alveolar oedema => Bat wing
B-lines => pulmonary oedema
Cardiomegaly (more than half of the thoracic cavity in PA)
Dilated upper lobe vessels
pleural Effusions

29
Q

What ECG findings would be concerning in a patient with ATN?

A

Patient with ATN is at risk of hyperkalemia
ECG Changes : Tented T waves, flattened P waves, and widened QRS complex before ending with sine wave pattern and V.fib

30
Q

What grading scale would you use for AKI? What is it based on?

A

KDIGO
based on creatinine levels and urine output
1 = Creatinine 1.5-1.9x baseline, <0.5ml/kg/hr for <12 hrs
2 = Creatinine 2-2.9x baseline, <0.5ml/kg/hr for >12hrs
3 = Creatinine 3x baseline, <0.3 ml/kg/hr

31
Q

In AKI, what are the indications for Renal Replacement Therapy (RRT)?

A

AEIOU mnemonic
Acidosis => pH<7.1
Electrolyte imbalance => Hyperkalemia >7mmol/L or ECG change
Ingestion of toxins/poisons
fluid Overload despite dialysis use
Uremic symptoms (pruritis, confusion, anorexia, vomiting, asterixes)

32
Q

What diuretic would you use for pulmonary oedema or fluid overload?

A

Furosemide

33
Q

What are the complications of AKI?

A

Chronic renal failure
Hyperkalemia (>7)
Pulmonary Oedema (CXR ABCDE)