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Pathology by week > W14 - AKI & CKD > Flashcards

W14 - AKI & CKD Flashcards

1
Q

AKI is a rapid reduction in kidney function, leading to inability to …. 3 things - list them.

A

Maintain electrolyte (1), acid-base (2), and fluid (3) homeostasis

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2
Q

NHS England defines stages of AKI based on what measurement?

A

Serum Creatinine (sCr)

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3
Q

Define the stages of AKI

A

AKI Stage 1: Increase in sCr by ≥26 µmol/L, or by 1.5 to 1.9x the reference sCr

AKI Stage 2: Increase in sCr by 2.0 to 2.9x the reference sCr

AKI Stage 3: Increase in sCr by ≥3x the reference sCr, or increase by ≥354 µmol/L

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4
Q

The type of AKI is divded into … (3)

A
  1. Pre-renal
  2. Intra-renal
  3. Post-renal
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5
Q

What is the hallmark of pre-renal AKI?

A

Persistent reduced renal perfusion despite normal adaptive mechanisms (i.e. activation of RAS, release of vasopressin, activation of sympathetic system = vasoconstriction, increased C.O., and renal sodium retention)

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6
Q

Causes (5) of pre-renal AKI

A
  1. True volume depletion
  2. Hypotension
  3. Oedematous states
  4. Selective renal ischaemia
  5. Drugs affecting glomerular blood flow ((NSAIDs, calcicneurin inhibitors, ACEi, or ARBs, diuretics)
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7
Q

Describe the 5 classes of drugs that predispose to pre-renal AKI and describe MOA of each

A
  1. NSAIDs - decrease afferent arteriolar dilatation
  2. Calcineurin inhibitors - as above
  3. ACEi - decrease efferent arteriolar constriction
  4. ARBs - as above
  5. Diuretics – affect tubular function, decrease preload
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8
Q

A 68 year old man with previously normal renal function is found to have a creatinine of 624μmol/l. Renal ultrasound shows the following appearance in both kidneys. What is the likely cause of his AKI?

A.Right-sided kidney stone

B.Left ureteric transitional cell carcinoma

C.Membranous glomerulonephropathy

D.Benign prostatic hypertrophy

E.Amyloid

A

Classic image of hydronephrosis = some obstruction to the kidneys = most likely here is

D.Benign prostatic hypertrophy

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10
Q

What is the hallmark of post-renal AKI?

A

Hallmark of post-renal AKI is a physical obstruction to urine flow

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11
Q

Give 3 main specific causes of post-renal AKI

A
  1. Ureteric obstruction (i.e. renal calculi)
  2. Urethral obstruction (i.e. prostatic obstruction)
  3. Blocked urinary catheter (i.e. clots)
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12
Q

What is the pathophysiology behind post-renal obstruction leading to AKI?

A

Obstruction results in increased tubular pressure

GFR is dependent on hydraulic pressure gradient

reduced gradient = immediate decline in GFR = creatinine will rise acutely (likely to 1000s)!

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13
Q

What 3 structural damages could occur due to prolonged post-renal obstruction?

A
  1. Glomerular ischaemia
  2. Tubular damage
  3. Long-term interstitial scarring

therefore imp to immediately relief obstruction!

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14
Q

Intra-renal AKI = What are 4 parts of the nephron that could be affected?

A
  1. Vascular disease (i.e. vasculitis)
  2. Glomerular disease (i.e. glomerulonephritis)
  3. Tubular disease (i.e. ATN)
  4. Interstitial disease (i.e. analgesic/NSAID nephropathy)
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15
Q

Patient has new onset AKI. What is the likely diagnosis?

A

Rhabdomyolysis

Patient who potentially has fallen, lots of myoglobin release, which has blocked their tubule and caused AKI

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16
Q

A 40 year old female presents with a rash and AKI is diagnosed. What is the most likely cause of her renal failure from the following list?

A.NSAIDs

B.Systemic vasculitis

C.Amyloidosis

D.Tumour lysis syndrome following chemotherapy for lymphoma

E.Myeloma

A

B. Systemic vasculitis

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17
Q

Name 2 endogenous and 3 exogenous toxins that cause direct tubular injury in kidneys

A

Endogenous toxins

  1. Myoglobin
  2. Immunoglobulins

Exogenous toxins - contrast, drugs

  1. Aminoglycosides (gentamicin)
  2. Amphotericin (strong antifungal)
  3. Acyclovir
20
Q

The top 5 causes of AKI in the world are:

A
  1. Decreased renal perfusion
  2. Medications
  3. Radiographic contrast media
  4. Post-operative
  5. Sepsis

essentially all pre-renal

21
Q

What two measures do we use to define severity of AKI?

A
  1. serum creatinine (to get eGFR)
  2. Urine output
22
Q

How many stages of CKD are there? Describe each

A

Stage 1 => kidney damage with normal GFR (>90ml/min)

Stage 2 => mild reduced GFR (60-89ml/min)

Stage 3 => moderate reduced GFR (30-59ml/min)

Stage 4 => severe reduced GFR (15-29ml/min)

Stage 5 => end-stage kidney failure (<15 or dialysis)

23
Q

Other than GFR, what other parameter is used to categorise CKD?

A

Albumin:creatinine ratio (ACR) - checks to see amount of albumin (protein) in urine.

The higher the ACR the worse the prognosis

24
Q

Name the commonest (6) causes of CKD

A

Commonest are:

  1. Diabetes
  2. Atherosclerotic renal disease
  3. Hypertension
  4. Chronic Glomerulonephritis
  5. Infective or obstructive uropathy
  6. Polycystic kidney disease
25
Q

What are the consequences (4) of CKD?

(NB: think of normal functions of kidney that are lost)

A
  1. Failure of homeostatic function:

- ACIDOSIS

- HYPERkalaemia

  1. Failure of hormonal function:
    - ANAEMIA

- RENAL BONE DISEASE

  1. CVS disease:

- VASCULAR CALCIFICATION

- URAEMIC CARDIOMYOPATHY

  1. ultimately uraemia and death
26
Q

As a result of renal acidosis (H+ retention) in CKD, we get metabolic acidosis. What does this cause (3) in the body?

How do we treat it?

A
  1. Muscle and protein degradation
  2. Osteopenia due to mobilisation of bone calcium
  3. Cardiac dysfunction

Treatment => oral sodium bicarbonate (help them buffer)

27
Q

Regarding hyperkalaemia, which of the following is true:

A. It can lead to ECG changes such as peaked p waves and flattened t waves.

B. In those with CKD, dietary intake is a major cause and high potassium levels are found in foods such as milk, chocolate, dried fruits and tomatoes.

C. NSAIDs can lower potassium levels

D. Hyperaldosteronism is a common cause

E.All of the above

A

B = true

A = flattened p waves, peaked T waves

C = NSAIDs can increase K+ levels

D = Conns would cause a LOW potassium

28
Q

Renal vascular lesions are mostly vascular calcifications rather than traditional lipid-rich atheromas in those with CKD - true or false?

A

True

29
Q

What are the 3 phases of uraemic cardiomyopathy seen in CKD?

A
  1. LV hypertrophy
  2. LV dilatation
  3. LV dysfunction
30
Q

As a result of progressive decline in EPO-producing cells with loss of renal prenchyma, we get anaemia of chronic renal disease.

When would this be noted usually?

What do the RBCs look like?

A
  1. usually when GFR <30ml/min
  2. Normochromic, normocytic anaemia

(always exclude iron, B12, and folate deficiency)

31
Q

How do we treat anaemia caused by CKD?

A

3 Erythropoiesis-stimulating agents (ESAs) are available for use

32
Q

Your patient with CKD has been started on an ESA but does not respond. What could be the cause?

A.Iron deficiency

B.TB

C.Malignancy

D.B12 and folate deficiency

E.Hyper-parathyroidism

F.Any of the above

A

F. any of the above

35
Q

Which of the following are contraindications to kidney transplantation?

  • HIV positive
  • BMI >30
  • Active sepsis
  • Aged >65
  • Any malignant disease
A
  • HIV positive = NO
  • BMI >30 = NO
  • Active sepsis = YES
  • Aged >65 = NO
  • Any malignant disease = NO

Pathology by week (70 decks)

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