deck_1665492 Flashcards

(59 cards)

1
Q

What is Oliguria?

A

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

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2
Q

What is anuria?

A

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

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3
Q

Give three causes of acute kidney injury

A

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

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4
Q

What is pre-renal acute kidney injury caused by?

A

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

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5
Q

Give two over arching causes of pre-renal AKI

A

• Reduced effect ECF volumeImpaired renal autoregulation

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6
Q

Give three overarching causes of reduced effective ECF volume

A

• Hypovolaemia • Systemic vasodilation • Cardiac failue

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7
Q

Give two causes of hypovolaemia

A

• Blood loss • Fluid loss

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8
Q

Give three causes of systemic vasodilation

A

• Sepsis • Cirrhosis • Anaphylaxis

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9
Q

Give three causes of cardiac failure

A

• LV dysfunction • Valve diseaseTamponade

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10
Q

Give two causes of impaired renal autoregulation

A

• Preglomerular vasoconstriction • Postglomerular vasodilation

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11
Q

Give four causes of preglomerular vasoconstriction

A

• Sepsis • Hypercalcaemia • Hepatorenal syndrome • Drugs - NSAIDS

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12
Q

Give two causes of post glomerular vasodilation

A

• ACE inhibitors • Angiotensin 2 antagonists

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13
Q

What is post renal AKI?

A

• Injury as a result urine flow obstruction

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14
Q

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

A

• Ureters • Bladder • Urethra

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15
Q

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

A

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

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16
Q

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

A

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

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17
Q

How large must a calculi be to stop it passing?

A

> 10mm

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18
Q

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

A

• Congenital • Ureteric stricture

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19
Q

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

A

Chronic kidney injury

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20
Q

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

A

• Pelviureterteric neuromuscular dysfunction • Megaureter • Neurogenic bladder

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21
Q

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

A

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

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22
Q

Give three causes of intrinsic AKI

A

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

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23
Q

What are the two main causes of acute tubular necrosis?

A

• Severe acute ischaemia • Toxic acute tubular necrosis

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24
Q

What is severe acute ischaemia caused by?

A

• 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 erthyrematosusVasculitis
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 refillHypotension
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’ patternAsystole
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 withGLOMERULONEPHRITIS?
• 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 perfusionAvoid nephrotoxins
59
When is dialysis indicated?
When kidneys can no longer adequately excrete salt, water and potassium