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Flashcards in Week 9 - Acute Kidney injury Deck (55):
1

How is GFR measured?

-Measure in serum creatinine

2

Why is AKI treated as a medical emergency?

-Delayed treatment leads to irreversible renal failure

3

What are the three groups of causes of AKI?

-Pre-renal
-Intrinsic renal
-Post-renal

4

What type of injury cause pre-renal failure?

-Anything which causes volume depletion to the kidney eg heart failure, cirrhosis

5

What type of diseases cause intrinsic renal AKI?

-Any kind of necrosis or ischaemia which affects the parenchyma eg glomerulonephritis, Acute Tubular Necrosis

6

What type of injury causes post-renal AKI?

-Anything which obstructs the urinary tract eg stones, prostate hyperplasia

7

What is the major cause of AKI?

-Acute tubular necrosis

8

Describe the pathophysiology of pre-renal AKI

-Reduced renal blood flow reduces GFR
-There is no cellular damage so kidneys work hard to restors bloodflow and avidly resorb salt and water

9

Does pre-renal AKI respond to fluid resuscitation?

Yes

10

Describe urine production in pre-renal AKI

-Little and concentrated because reabsorbing fluid

11

Why is hypertension significant in pre-renal AKI?

-Blood pressure may seem adequate however the patient may normally have high BP so their current BP is low and the person is at risk of pre-renal AKI

12

Describe autoregulation in pre-renal AKI

-Reduced renal perfusion causes vasodilation of afferent arteriole to increase renal blood flow
-Vasoconstriction of efferent arteriole to increase renal blood pressure
-Attempts to maintain GFR

13

Why does AKI occur in pre-renal states?

-Autoregulation becomes overwhelmed and cannot maintain GFR

14

At what pressures is autoregulation able to work?

-80-180mmHg

15

Name 2 drugs which can override autoregulation and explain why?

-NSAIDs -> inhibit prostaglandin production -> inadequate vasodilation of afferent arteriole
-ACE inhibitor -> inhibits angiotensin II which acts as a vasoconstrictor of efferent arteriole

16

What develops from pre-renal AKI if the underlying cause is not treated?

-Acute tubular necrosis

17

What are the major causes of acute tubular necrosis?

-Ischaemia
-Necrosis
-Sepsis

18

What is acute tubular necrosis?

-Injury to proximal tubular cells which results in inability to resorb salts and water efficiently or expel excess water

19

Does ATN respond to fluid resuscitation?

-Sometimes but high risk of fluid overload

20

Is AKI reversible?

-Potentially yes

21

When does mortality significantly increase in AKI?

-If dialysis is required

22

Describe the pathophysiology of ischaemic necrosis

-The PCT is the most susceptible area to hypoxia as it has the higest O2 demand
-Any cause of hypoxia to the cells results in injury and the cells can no longer function

23

Describe the urine produced in ATN

-Often copious and dilute

24

Describe the pathophysiology of toxin ATN

-Nephrotoxins damage epithelial cells lining tubules and cause shedding into lumen
-ATN is much more likely to occur if there is reduced perfusion and presence of a nephrotoxin

25

Name some endogenous nephrotoxins

-Myoglobin, bilirubin, urate

26

NAme some exogenous nephrotoxins?

-Endotoxin
-X-ray contrast
-drugs eg gentamycin, NSAIDs
-Poisons

27

What is rhabdomyolysis and why can it cause AKI?

-Muscle necrosis, often due to crush injuries, causes release of myoglobin
-Myoglobin is filtered at the glomerulus and is toxic to tubule and may cause obstruction -> causes AKI

28

What is characteristic of rhabdomyolysis?

-Produces black urine

29

What is acute glomerulonephritis?

-Immune diseases which affect the kidney
-Can by primary and only affect the kidneys or secondary as part of a systemic process

30

Name some secondary glomerulonephritis

-Systemic lupus erythema
-Vasculitis

31

What is wegners granulomatosis?

-Rapid progressive glomerulonephritis with granulomatosis and polyangitis

32

Name a primary glomeruonephritis

-IgA nephropathy

33

Name 2 causes of acute tubulo-interstitial nephritis

-Infection eg acute pyelonephritis
-Toxin-induced eg NSAIDs

34

Describe the pathophysiology of post-renal AKI

-Obstruction which blocks both kidneys causes an increase in intraluminal pressure as urine is continually being produced
-This causes dilation of renal pelvis (hydronephrosis)
-Decreased renal function

35

What 3 groups can cause obstruction AKI?

-Within the lumen eg stones, tumours
-Within the wall, stricture post TB, congenital megaureter
-Pressure from outside eg enlarged prostate, tumour, aortic aneurysm

36

What criteria must stones meet to cause AKI?

-Must be in neck of bladder, urethra or both ureters

37

What are the common signs of renal stones?

-Loin to groin pain
-Haematuria
-Cannot lie still

38

What U+E results would indicate AKI?

-Hyponatraemia
-Hyperkalaemia
-High urea
-High creatinine
-Hypocalcaemia and hyperphosphataemia

39

What ECG changes signify hyperkalaemia?

-Tall, tented T waves
-Small/absent P waves
-Increased PR interval
-Widened QRS

40

Describe signs which would point towards the patient being volume depleted

-Cool peripheries, increased pulse, low bp, dry axillae

41

Describe signs which would point towards the patient being fluid overloaded

-Gallop rhythm, pulmonary oedema, peripheral oedema

42

What is mandatory in every patient with AKI?

-Urinalysis using dipstick for blood, protein and leukocytes

43

Describe how AKI is investigated

-Urine dipstick, culture and chemitry
-USS, CXR
-Biopsy if appropriate

44

When do you use USS in AKI?

-Post-renal or pre-renal/ATN not improving

45

When do you biopsy in AKI?

-Pre and Post-renal ruled out
-Confident ATN diagnosis cannot be made
-SIRS present

46

What is the main priority in AKI?

-BP and blood vol followed by pH and hyperkalaemia then watse and drug metabolism

47

How do you prevent AKI?

-Identify risk factors and monitor at-risk patients
-Ensure adequate hydration
-Avoid nephrotoxins

48

Describe some risk factors for developing AKI

-Advanced age
-CKD
-Heart/liver disease
-Sepsis/critical illness
-Burns/trauma

49

How do you manage patients in volume overload?

-Restrict dietary Na and water intake

50

How do you manage hyperkalaemia?

-Calcium gluconate
-IV insulin + dextrose
-Restrict dietary K
-Stop K sparing diuretics and ACEI

51

What are indications of AKI for dialysis?

-High K+ non-responsive to treatment
-Fluid overload despite diuretics
-Metabolic acidosis where NaHCO3 not appropriate
-Presence of dialysable nephrooxin
-Signs of uraemia

52

Describe some signs of uraemia

-Pericarditis
-Reduced consciousness
-Intactable N&V

53

Describe the prognosis of uncomplicated ATN

-Expect recovery in 2-3 weeks
-Mortality varies from 30-80%

54

Patients who experience AKI are at risk of what in later life?

-Higher risk of death for 1 year
-Higher risk of developing CKD

55

What is acute kidney injury?

-Clinical syndrome characterised by an abrupt decline in GFR, upset of ECF volume, electrolyte and acid-base homeostasis and accumulation of nitrogen waste products