Session 10 - Acute Kidney Injury Flashcards Preview

Semester 3 - Urinary > Session 10 - Acute Kidney Injury > Flashcards

Flashcards in Session 10 - Acute Kidney Injury Deck (59):
1

What is Oliguria?

• Little urine
• Less than 500ml of urine/day or less than 20ml/hour

2

What is anuria?

• No urine
• Less than 100ml of urine/day
• Indicates blockage of urine flow

3

Give three causes of acute kidney injury

• Pre-renal disease
○ Decreased perfusion
• Post-renal failure
○ Obstruction
• Intrinsic Renal Failure
○ Dame to kidney

4

What is pre-renal acute kidney injury caused by?

• A reduction in renal perfusion
• If not treated promptly acute tublar necrosis will develop

5

Give two over arching causes of pre-renal AKI

• Reduced effect ECF volume

Impaired renal autoregulation

6

Give three overarching causes of reduced effective ECF volume

• Hypovolaemia
• Systemic vasodilation
• Cardiac failue

7

Give two causes of hypovolaemia

• Blood loss
• Fluid loss

8

Give three causes of systemic vasodilation

• Sepsis
• Cirrhosis
• Anaphylaxis

9

Give three causes of cardiac failure

• LV dysfunction
• Valve disease

Tamponade

10

Give two causes of impaired renal autoregulation

• Preglomerular vasoconstriction
• Postglomerular vasodilation

11

Give four causes of preglomerular vasoconstriction

• Sepsis
• Hypercalcaemia
• Hepatorenal syndrome
• Drugs - NSAIDS

12

Give two causes of post glomerular vasodilation

• ACE inhibitors
• Angiotensin 2 antagonists

13

What is post renal AKI?

• Injury as a result urine flow obstruction

14

What are the three sites at which urine flow can be blocked, causing post renal AKI?

• Ureters
• Bladder
• Urethra

15

What are three places obstructions can be at each particular site in post renal AKI?

• Within the lumen
• Within the wall
• Pressure from outside

16

Give four causes of blockage within the wall of the ureter, bladder or urethra

• Calculi
• Blood clot
• Papillary necrosis
• Tumour of renal pelvis, ureter or bladder

17

How large must a calculi be to stop it passing?

>10mm

18

Give two causes of obstruction within the wall of the ureter, bladder or urethra

• Congenital
• Ureteric stricture

19

What does obstruction with the wall of the ureter, bladder or urethra usually cause other than acute post renal AKI?

Chronic kidney injury

20

Give three congenital causes of obstruction within the wall of the ureter, bladder or urethra

• Pelviureterteric neuromuscular dysfunction
• Megaureter
• Neurogenic bladder

21

Give five causes of pressure from outside causng post-renal AKI

• Prostatic hypertrophy
• Malignancy
• Aortic aneurysm
• Diverticulitis
• Accidental ligation of ureter

22

Give three causes of intrinsic AKI

• Acute tubular necrosis
• Glomerular and arteriolar disease
• Acute tubule-interstitial

23

What are the two main causes of acute tubular necrosis?

• Severe acute ischaemia
• Toxic acute tubular necrosis

24

What is severe acute ischaemia caused by?

• Pre-renal fall in perfusion, causing tubular necrosis

25

What is toxic acute tubular necrosis?

• Nephrotoxins damage the epithelial cells lining the tubules and cause cell death
• Nephrotoxins can be endogenous or exogenous

26

What is the most common cause of acute tubular necrosis?

• Where there is toxic acute tubular necrosis AND severe acute iscaemia

27

Name three endogenous nephrotoxins

BUM
• Bilirubin
• Urate
• Myoglobin

28

Give four exogenous causes of ATN

• Endotoxin
• X-ray contrast
• Drugs
• Other poisons

29

Give three main drugs which are exogenous nephrotoxins

• ACE inhibitors
• NSAIDs
• Aminoglycosides

30

How are NSAIDs toxic to the kidney?

• Prostaglandins usually causes vasodilation of afferent arterioles in renal autoregulation
• NSAIDs inhibit prostaglandin production by inhibition of COX
• Unopposed vasoconstriction of afferent arteriole occurs -> Reduced glomerular perfusion pressure -> AKI

31

Why are ACE inhibitors exogenous nephrotoxins?

• Angiotensin II has a key role in homeostatic control of kidney blood flow
• Efferent arteriole constriction
• ACE inhibtors remove this effect, decreasing GFR

32

What will you see in Acute Tubular Necrosis?

• Muddy brown casts in urine
• Fractional excretion of Na+ >3%

33

How do you calculate fractional excretion of Na?

• (Na (urine) x Cr (plasma)/Cr (urine) x Na (plasma) ) x 100

34

Give two types of glomerular and arteriolar disease

• Primary acute glomerulonephritis
• Secondary acute glomeurlonephritis

35

What is acute glomerulonephritis?

• Immune disease affecting glomerulus (See session 9)

36

Give two causes of secondary acute glomerulonephritis?

• Systemic lupus erthyrematosus

Vasculitis

37

What is acute tubulo-interstitial nephritis? Give two causes

• Inflammation of the kidney intersitium
• Acute pyelonephritis and drugs

38

What are the three questions that should be asked when treating a patient with AKI?

• Are the kidneys underperfused? Pre-renal injury
• Are nephrotoxins implicated? Direct renal injury
• Is there a renal tract obstruction? Post-renal injury

39

If kidneys are underperfused, what are two main causes?

• Shock
• Severe vascular disease

40

What are the three main types of shock?

• Hypovoleamic
• Septic
• Cardiac

41

What is the main cause of severe vascular disease causing AKI?

Emboli

42

What are three main possible nephrotoxins in direct renal injury?

• Drugs
• Sepsis (endotoxins)
• Myoglobin

43

What is one disease you can NEVER forget which also causes direct renal injury?

• UTI progressing to pyelonephritis

44

Give five signs of cardiac failure

• Gallop rhythm
• Raised BP
• Raised JVP
• Pulmonary oedema – Basal crackles and dyspnoea
• Peripheral oedema (Sacral/ankle)

45

Give five signs of sepsis

• Pyrexia and rigors
• Vasodilation, warm peripheries
• Bounding pulse
• Rapid capillary refill

Hypotension

46

Give six signs of a urinary tract obstruction

• Anuria
• Single functioning kidney
• History of renal stones, prostatism or previous pelvic/abdominal surgery
• Palpable bladder
• Pelvic/abdominal masses
• Enlarged prostate (DRE)

47

What signs will you see in ALL AKI?

• Increased serum urea and creatinine
• Hyperkalaemia
• Hyponatraemia
• Hypocalcaemia
• Hypophosphataemia

48

What investigations are peformed in AKI?

• ECG
• Urine tests - Dipstick and microscopy
• Soluble immunological tests
• Imaging
• Biopsy

49

What ECG changes will you see in hyperkalaemia?

• Tall T waves
• Small/Absent P waves
• Increase P-R interval
• Wide QRS complex
• ‘sine wave’ pattern

Asystole

50

What do you look for in dipstick tests?

• Blood
• Protein
• Leucocytes

51

Will there be proteinuria/haematuria/any abnormal microscopy in the urine of someone with PRE-RENAL AKI?

• No proteinuria
• No haematuria
• Hyaline cast in urine - Aggregations of protein seen in concentrated urine (normal sign, but will be present on every urination)

52

Will there be proteinuria/haematuria/any abnormal microscopy in the urine of someone with ACUTE TUBULAR NECROSIS

• No proteinuria
• No haematuria
• Muddy brown casts in urine

53

Will there be proteinuria/haematuria/any abnormal microscopy in the urine of someone with

GLOMERULONEPHRITIS?

• Heavy proteinuria
• Heavy haematuria
• RBC casts

54

What soluble immunological tests can you do in AKI?

• Look for ANA (anti-nuclear antibody)
○ Indication for SLE
• Look for ANCA (anti-neutrophil cytoplasmic antibody (ANCA)
○ Systemic vasculitis
• Look for anti-glomerular basement membrane antibodies

Goodpasture's disease

55

What are two imagine techniques used in AKI?

• Ultrasound
○ Renal size
○ Hydronephrosis
○ Presence of obstruction
• Chest X-ray
○ Pulmonary oedema

56

What is the treatment for pre-renal AKI

• Volume correction
○ Hypovolaemia -> Fluids
○ Heart failure -> Diuretic

57

What is the treatment for post-renal failure?

• Urological intervention to re-establish urine flow

58

What is the treatment for acute tubular necrosis

• Maintain good kidney perfusion

Avoid nephrotoxins

59

When is dialysis indicated?

When kidneys can no longer adequately excrete salt, water and potassium