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Lucy Knox - Year 2.5 > 227 - Acute Renal Failure > Flashcards

227 - Acute Renal Failure Flashcards

1
Q

If this marker is high it suggests a poor prognosis / high mortality in AKI

A

High serum creatinine

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2
Q

What criteria is used for rating severity of AKI?

A

RIFLE criteria
GFR/Cr, urine output

Affected by age, DM, high BP, CCF

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3
Q

What extra-renal systems does AKI affect?

A

Pulmonary (pul oedema, ARDS, Leukocyte invasion, heamorrhage)

CNS (inflam reaction, altered conscious level, acidosis + electrolyte imbalence - confusion, convulsions, coma)

Cardiac (electrolyte imbalance, uraemic toxins, acidosis.. sympathetic NS - increase Bp, pericarditis, arrhythmias, Mi)

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4
Q

The causes of AKI are split into what 3 domains?

A

Pre-renal
Intrinsic
Post-renal

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5
Q

Describe how pre-renal issues can cause AKI

A

GFR reduced ↓ , due to haemodynamic disterbances - so causes ↓ globerular filtration.

No cellular injury

IF you reverse haemodynamic factors - should revert to ok

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6
Q

List 4 pre-renal causes of AKI

A

Intravascular vol depletion
↓ effective blood volume (burns)
Altered intrarenal haemodynamics (dehydration, sepsis)
3rd space sequestration (bowel obstruction)

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7
Q

List 3 intrinsic causes of AKI

A

Acute tubular necrosis (85%)
Radiocontrast nephropathy
Acute tubulo-interstial nephritis

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8
Q

What can cause acute tubular necrosis?

A

50% due to ischaemia - ↓bp, sepsis, cardiopulmonary arrest, bypass

35% nephrotoxic - drugs (aminoglycosides, radiocontrast, ACEi, NSAIDS) or pigment (Rhabdomyolysis, heamolysis)

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9
Q

How long does acute tubular necrosis last for?

A

Recover in 1 week due to proliferation and differentiation

Mortality linked with number of other failed organs

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10
Q

When might you be at risk of radiocontrast nephropathy?

A

When you need IV or intra-arterially injected contrast (special CT scans)

Not oral contrast or MRI contrast

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11
Q

Why can contrast cause nephropathy?

A

Contrast is hypertonic, so can induce transient vasodilation then constriction - can cause renal ischaemia.

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12
Q

How can you prevent contrast nephropathy?

A

Give lots of fluid - before and during

Use low osmolality contrast

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13
Q

What are the features of acute tubulo-interstitial nephritis?

A

An allergic reaction (so high mast cells and eosinophils)
Drug induced or infection mediated

  • Get fever, rash, arthralgia, eosinophila
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14
Q

What investigation can confirm acute tubulo-interstitial nephritis?

A

A biopsy - will show cellular infiltrates

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15
Q

What can cause post renal AKI?

A

An obstruction

- stone, necrosis, clot, TCC, stricture, fibrosis, tumour, aortic aneurysm

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16
Q

What are the features of urine in someone with post-renal AKI?

A

Dilute (can’t be concentrated as well)

Acidification is imparied - high blood acid and alkaline urine

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17
Q

What are 2 life threatening complications of AKI?

A

Metabolic acidosis

Hyperkaleamia

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18
Q

Describe metabolic acidosis in AKI

A

Can have a normal anion gap (bicarb is lost) or increased anion gap (acid is overproduced)

Get muscle weakness, altered mental state, kasmail breathing, high potassium and low BP

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19
Q

Describe how hyperkalemia occurs in AKI

A

When the pH of blood is low, H+ moves intracellularly
K+ moves out of cells to help keep the + balance
-> too much K+ in the blood

= muscle weakness, cardiac issues, big T waves (lots of pot lots of tea), wide QRS, bradycardia

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20
Q

How do you treat hyperkaleamia in AKI?

A

Treat cause
Give fluids
Correct acidosis
Protect heart - IV Ca Gluconate
Shift K+ back into cells - IV dextrose insulin
Reduce K+ absorption in GI tract - cation exchange resin

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21
Q

What is Rhabdomyolysis?

A

AKI caused by muscle necrosis releasing intracellular constituents. The AKI then causes electrolyte imbalance

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22
Q

How does Rhabdomyolysis cause AKI?

A

Haem pigment casts obstruct tubules - proximal tubular injury by heam iron

+ volume depetion due to swelling of damaged muscle

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23
Q

What are the signs and blood abnormalities of rhabdomyolysis?

A

Red/brown urine (as pigmented granular casts and supernatant in)

High serum enzymes - CK and LDH
Hifh K+, phosphate and uric acid
Low Ca (as goes to damaged muscles)

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24
Q

What could it mean if Ca was high in someone with known rhabdomyolysis?

A

They might be recovering, the excess Ca taken up by damaged muscles is released as it heals

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25
Q

What can cause rhabdomyolysis?

A

Trauma - crush, struggle, immobilisation, compression

Non-traumatic - marathon, hot weather, low K+, convulsions, low phosphate, alcohol, opiates, statins, cyclosporin, infections, DKA

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26
Q

How can you prevent rhabdomyolysis from occurring?

A

Fluid repletion
Forced alkaline diuresis - if you increase the pH of urine then less myoglobin precipitates with tamm-horsfall protein - reduces free radical release - better
Mannitol forced diuresis - osmotic diuretic. help flush out.

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27
Q

What is myeloma kidney?

A

A plasma disorder characterised by monoclonal immunoglobulin proliferation + marrow infiltration

Causes heam abnormalities - anaemia
Immune paresis
Renal injury

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28
Q

How does myeloma kidney lead to renal injury?

A

Light chain Ig can be filtered by glomeruli and reabsorbed by the PCT, but they can block it - obstruction - AKI

The light chain Igs also can bind to tamm-horsfall protein and precipitate into the tubules - obstruction and ? rupture - AKI

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29
Q

What signs are seen in myeloma kidney?

A

bone pain, weight loss, pallor, hyperviscosity - headaches, high BP, visual issues, convulsions

  • Renal failure, anaemia, high calcium and low platlets
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30
Q

What is the 1st line investigation for myeloma kidney?

A

SPEP electrophoresis

  • look at the gamma antibody peaks - will see an abnormal high peak
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31
Q

What investigations can be done to confirm myeloma kidney?

A 
SPEP electrophoesis (1st line)
immunofixation
Free light chain assay
Kidney biopsy
Bone marrow biopsy?
Xray - see punched out lesions
32
Q

What are the treatment options for myeloma kidney?

A

You try to target each issue:

  • cast nephropathy - IV fluid, plasma exchange, or reduce production - chemo + steroids
  • hyperuricaemia - xanthine oxidase inhibitors, urate oxidase, fluid
  • hypercalcaemia - fluid + bisphosphonates
  • Hyper-viscosity - fluid, plasma exchange
33
Q

Many drugs affect the kidneys. Which can cause damage by volume depletion?

A

Excessive laxatives
Loop diuretics (furosemide, benetanide)
NSAIDS

34
Q

Many drugs affect the kidneys. Which can cause damage by altering renal haemodynamics?

A

ACE inhibitors
A2RBs (angiotensin II receptor blockers

  • have vasodilator effects on efferent glomerular arterioles
35
Q

Many drugs affect the kidneys. Which can cause damage by causing hypercalcaemia?

A

Calcium preparations

Vit D in a toxic dose

36
Q

Many drugs affect the kidneys. Which can cause damage by hyperuricemia?

A

Chemo for bulky tumours

37
Q

Many drugs affect the kidneys. Which can cause damage by causing hyperkalemia?

A 
ACEi
A2RBs
Spironolactone
amiloride (K+ sparing diuretic)
NSAIDS
38
Q

Many drugs affect the kidneys. Which can cause damage by causing hypokalemia?

A 
loop diuretics
Thiazide diuretics (bendroflumethiazide)
39
Q

Many drugs affect the kidneys. Which can cause damage by increasing serum creatinine?

A

Trimethoprim
Cimetridine

  • block Cr secretion
40
Q

Many drugs affect the kidneys. Which can cause damage by irreversibly damaging the kidneys?

A

Aminoglycosides (gentamicin)

NSAIDS

41
Q

Many drugs affect the kidneys. Which can cause damage by increasing CK - causing rhabdomyolysis?

A

Statins + Calcineurin inhibitors (cyclosporin)

Particularly together

42
Q

Renal failure affects drug processing.

Which drug is affected by: volume depletion ?

A

Gentamicin - has a small vol of distribution, so if volume depletion, big effect

43
Q

Renal failure affects drug processing.

Which drug is affected by: altered protein binding?

A

Phenytoin - more free drug becomes available as proteins it usually binds to (albumin) are reduced, or other things (eg. urea) bind competitively to them.

44
Q

Renal failure affects drug processing.

Which drug is affected by: a reduction in drug metabolism?

A

Insulin - as kidney is place of phase I and II drug metabolism - so less broken down, increased serum conc

45
Q

Renal failure affects drug processing.

Which drug is affected by: reduced elimination

A

Renally excreted drugs - morphine

Increased half life - give lower dose

46
Q

Renal failure affects drug processing.

Which drug is affected by: uraemia

A

uraemia alters bodys response to drugs

  • increases sensitivities to CNS acting drugs (benzos)
  • increases GI bleed risk (NSAIDS)
  • increases hyperkalamia risk (K sparing diuretics - amiloride)
47
Q

Renal failure affects drug processing.

Which drug’s effect is lost?

A

Nitrofurantoin - needs to be excreted into the urinary tract to work.

48
Q

What can be checked in a urinalysis?

A

Chemical content
Protein content
Formed elements (Cells, RBCs, Fat, Casts)
Crystals

49
Q

How are casts formed in urine?

A

Formed in the DCT and collecting ducts by tubular microproteins (eg. tamm-horsfall)

50
Q

What makes casts in urine abnormal?

A

When cells get trapped in the casts

  • eg. RBC casts due to glomerulonephritis
  • WBC casts - pyelonephritis or interstitial damage
  • Fatty casts - nephrotic syndrome
51
Q

Name 4 crystals that can be found in urine?

A

Calcium oxalate
Triple Phosphate
Uric Acid
Cystine

52
Q

What shape are calcium oxalate crystals?

A

envelope

? stones present?

53
Q

What shape are triple phosphate crystals? Why do you get them?

A

Coffin lid - rectangle.

in a UTI + alkaline urine

54
Q

What do uric acid crystals suggest?

A

Gout, hyperuricaemia

55
Q

What is GFR?

A

Glomerular filtration rate

use a substance with constant levels that is only excrete by glomerular filtration - eg. urea or creatinine

56
Q

Does urea give an over or underestimation of GFR?

A

Underestimates - some reabsorbed

57
Q

Does creatinine over or underestimate GFR?

A

Overestimates.
It is freely filtered, but tubular secretion is altered by drugs (eg. trimethoprim)

If high muscle mass, more creatinine

58
Q

What is eGFR?

A

estimated glomerular filtration rate

Serum creatinine put into equation

adjusted for age, wt, gender, race

59
Q

What is hyponatremia?

A

Serum Na

60
Q

What signs can you get with hyponatremia?

A

Asymptomatic?

Nausea, confusion, headache, lethargy, convulsions, coma.

61
Q

What investigation findings would you find in someone with hyponatremia?

A

Low serum osmolality (usually)
High urine osmolality
If volume deplete, urinary Na 40

62
Q

What are the 3 groups causes of hyponatremia fit into?

A

High ADH state
Low ADH state
High plasma osmolality

63
Q

What high ADH states can cause hyponatremia?

A

Hypovolaemia - diarrhoea, vomiting, thiazide diuretics

Hypervolaemia - heart failure, liver cirrhosis, SIADH, ecstacy, pregnancy

64
Q

What LOW ADH states can cause hyponatremia?

A

renal failure
Polydipsia
Beer drinkers

65
Q

What high osmolality states can cause hyponatremia?

A

renal failure
hyperglycaemia
mannitol therapy
pseudohyponatramia

66
Q

How can you treat hyponatremia?

A

Treat cause!

fluid restriction and salt replacement

if severe: vasopressin receptor antagonist (tolvaptam), loop diuretics

67
Q

What can occur if you correct hyponatremia too quickly?

A

Osmotic demyelination syndrome

2-3 days later - dysarthria, dysphagia, paraparesis, confusion, behavioural issues.

68
Q

Where is prorenin produced?

A

Juxtaglomerular cells

69
Q

Where is renin stored?

A

Juxtaglomerular cells

70
Q

Where is angiotensin I produced?

A

liver + kidney

71
Q

Where is ACE produced?

A

Lung

72
Q

Where is aldosterone produced?

A

Adrenal cortex

73
Q

What prompts the release of renin?

A

Low renal blood flow

Increased sympathetic tone

74
Q

What does angiotensin II cause?

A

efferent renal arteriolar contraction

Peripheral vasoconstriction

75
Q

What does aldosterone do?

A

Activates Na/K pump in DCT - increases Na and water reabsoption

Lucy Knox - Year 2.5 (15 decks)

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