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Urinary System > Acute And Chronic Kidney Disease > Flashcards

Acute And Chronic Kidney Disease Flashcards

1
Q

What is AKI?

A

Clinical syndrome
Abrupt decline in actual GFR (days to weeks)
Upset of ECF volume, electrolytes and acid-base balance
Accumulation of nitrogenous waste products

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2
Q

Why is AKI difficult to diagnose?

A

Doesn’t present with a specific identifiable symptom

Measurements are not massively accurate either

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3
Q

What happens to serum creatinine as kidneys decline?

A

Kidney decline leads to increased serum creatinine

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4
Q

How do we define AKI through measurements?

A

Increased serum creatine > 26.5 micromoles/L within 48 hrs
Increased serum creatinine > 1.5 x their baseline in 7 days
Urine volume <0.5 ml/kg/h for 6 hours

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5
Q

Describe the staging of AKI

A

1 - 3 in increasing severity
1 = 1.5 - 2 times their baseline
2 = 2 - 3 times their baseline
3 = > 3 times their baseline

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6
Q

What are the types of AKI?

A

Pre-renal
Intrinsic renal
Post-renal

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7
Q

What are the causes of pre-renal AKI?

A

Blood supply compromised
Volume depletion
Heart failure
Cirrhosis

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8
Q

Give some renal causes of AKI

A 
Renal artery/vein occlusion 
Glomerulonephritis 
Intrarenal vascular 
Ischaemic ATN
Toxic ATN 
Interstitial disease
Intrarenal disease 
Intrarenal obstruction
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9
Q

What does ATN stand for?

A

Acute tubular necrosis

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10
Q

What type of AKI are the vast majority?

A

Pre-renal

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11
Q

90% of intrinsic renal causes of AKI are due to …

A

ATN

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12
Q

Give some general causes of AKI

A 
Infective
Diarrhoea 
Obstetric illness
Venoms
Malaria 
Dyes
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13
Q

Describe how pre-renal problems cause AKI

A

Actual GFR reduced due to decreased renal blood flow
No cell drainage
Kidney works hard to restore blood flow
Increased reabsorption of salt and water (lots of aldosterone and ADH)
RAAS activated
Responds to fluid resuscitation

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14
Q

Describe autoregulation of the kidneys

A

Keeps the kidneys between a minimum and maximum BP over which they can maintain a normal perfusion pressure
When hypertensive, these values shift to higher BPs (reset)

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15
Q

What is the SM response to decreased renal perfusion?

A

Vasodilation of afferent

Vasoconstriction of efferent

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16
Q

Why do NSAIDs make AKI worse?

A

Inhibition of production of prostaglandins
Cannot vasodilate in the arterioles of kidneys when required
Cannot regulate perfusion pressure

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17
Q

Why can ACEi make AKI worse?

A

Cannot vasoconstrict when need to

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18
Q

Give some causes of reduced ECF volume

A 
Hypovolaemia 
Blood loss
Fluid loss
Sepsis 
Cirrhosis 
Anaphylaxis 
LV dysfunction 
Valve disease
Tamponade
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19
Q

Give some causes of impaired renal autoregulation

A 
Sepsis 
Hypercalcaemia 
Hepatorenal syndrome 
NSAIDs
ACEi
AngII antagonists
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20
Q

What are the causes of ATN?

A

Ischaemia
Nephrotoxins
Sepsis

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21
Q

Why is ATN a misnomer?

A

As there is generally no tubular necrosis

But cells are damaged

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22
Q

Describe ATN

A

Damaged cells cannot reabsorbed salt and water efficiently
Or expel excess water
Aggressive fluid resuscitation risks fluid overload
Lost the ability to concentrate urine therefore urine comes out at the same rate no matter the volume of ECF

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23
Q

If dialysis is required, does the mortality of AKI increased or decreased?

A

Mortality increases

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24
Q

Which parts of the nephron are most susceptible to hypoxia?

A

S3 of PCT

Thick ascending limb LOH

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25
Describe damage in the kidneys due to nephrotoxins
Damage the epithelial cells lining the tubules and cause cell death and shedding into the lumen Can be endogenous or exogenous ATN more likely if reduced perfusion and a nephrotoxin
26
Give examples of endogenous nephrotoxins
Myoglobin Urate Bilirubin
27
In which treatment does urate build up?
Chemotherapy
28
Give some examples of exogenous nephrotoxins
Bacteria endotoxins Xray contrast Drugs (ACEi, aminoglycosides, NSAIDs) Poisons (weedkillers, antifreeze)
29
How does rhabdomylosis cause ATN?
Muscular necrosis releases myoglobin 'crush injury' In wars and natural disasters Can occur in drug users and elderly when cannot move Myoglobin is toxic to tubule cells and can also cause obstruction
30
Describe acute glomerulonephritis
Immune disease affecting the glomeruli | Can be primary or secondary
31
Give 2 types of rapidly progressing glomerulonephritis
Granulomatosis with polyangiitis | Crescenteric necrotising glomerulonephritis
32
Describe acute tubulo-interstitial nephritis
Caused by infection or toxins | Massive inflammatory infiltrate (lymphocytes)
33
What percentage of AKIs are post-renal causes?
5-10%
34
What is the general mechanism for post-renal AKI?
Obstruction most block both kidneys or a single functioning kidney Rise in intraluminal pressure Dilation of renal pelvis Decrease in renal function
35
Give some causes of post-renal AKI
Within lumen - stones, clots Within wall - strictures (eg. Post-TB) Pressure from outside - BPH, tumour, aortic aneurysm
36
Describe the serum changes common to all AKIs
Increased urea | Increased creatinine
37
What are the ECG changes of hyperkalaemia?
``` Tall T waves Small/absent P waves Increased P-R interval Wide QRS Sine wave pattern Asystole ```
38
What do we check to see if the patient is volume depleted?
``` Cool peripheries Increased pulse Decreased BP Postural hypotension Low JVP Reduced skin turgor ```
39
What do we assess when looking for fluid overload?
``` Gallop rhythm Increased BP Raised JVP Pulmonary oedema Peripheral oedema ```
40
Describe the Hx of a patient will post-renal AKI
``` Anuria A single functioning kidney Loin/supra-pubic pain Hx of stones Hx of prostration or previous pelvic/abdo surgery ```
41
What should we examine for in post-renal AKI?
Palpable bladder Pelvic/abdo masses Enlarged prostate (Blocked catheter)
42
What is essential to do for every patient with AKI?
Urinanalysis | Blood, protein, leukocytes
43
What features of a urinanalysis of AKI when suggest intrinsic renal disease?
Blood and/or protein
44
How do we image AKI?
Ultrasound scan - obstruction | CXR - fluid overload, infection
45
Name some preventative methods for AKI
``` Identify risk factors Monitor at risk patients Ensure adequately hydrated Avoid nephrotoxins Detect early and identify cause ```
46
Give some of the susceptibilities for AKI
``` Increased age CKD Heart disease Liver disease Diabetes mellitus Neurological impairment Cancer Previous AKI ```
47
Give some exposure risk factors for AKI
``` Dehydration/volume depletion Sepsis Critical illness Burns/trauma Cardiac surgery Emergency surgery Nephrotoxins Contrast ```
48
What is the management for AKI?
Treat fluid overload - restrict Na+ and water Treat hyperkalaemia with calcium gluconate, restriction of dietary K+, stop K+ sparing diuretics, ACEi etc, give dextrose and insulin, sodium bicarbonate Treat acidosis - protein restrict, sodium bicarbonate
49
What are the indications that an AKI patient needs dialysis?
``` Increased K+ Metabolic acidosis Fluid overload (All not responding to normal treatment) Presence of dialysable nephrotoxin Signs of uraemia ```
50
What is the prognosis for uncomplicated ATN?
Recovery in 2-3 weeks if no extra insults
51
What is the overall AKI mortality?
24%
52
What is the normal GFR range?
90 - 120 ml/min
53
How many nephrons do we have and how many do we need to survive?
2 million | Need 40,000 approx (2%) to survive
54
What is chronic kidney disease?
Long term condition Abnormal kidney function and/or structure The irreversible and sometimes progressive loss of renal function over a period of months to years
55
What is the commonest cause of CKD?
Unknown
56
Name some causes of CKD
``` Unknown Immunological - glomerulonephritis Infection - pyelonephritis Genetic - PCK, Alport Obstruction and reflux nephropathy Hypertension Vascular Systemic disease - diabetes, myeloma ```
57
What is the common end point for the kidneys of many CKDs?
Small, shrunken kidney With irregular outline Lots of fibrous scarring
58
Who should be screened by CKD?
Diabetes Hypertension Ischaemic heart disease
59
Who is CKD more common in?
Elderly Ethnic minorities Multi-morbid people Socially disadvantaged
60
What is CKD classification based on?
GFR
61
Describe the stages of CKD
``` G1 >90 G2 60-89 G3a 45-59 G3b 30-44 G4 15-29 G4 < 15 ```
62
Which measures of GFR are not very accurate?
> 60 GFR
63
Other than GFR, what other measurement can we look at?
ACR Albumin:creatinine ratio Higher it gets = worsened condition
64
What are the stages of ACR?
A1 < 3 A2 3 - 30 A3 > 30
65
What percentage of the adult population have CKD 3 or worse?
Approx 7%
66
Risk of death starts to increase when kidney function has declined by what percentage?
25% | Even though no symptoms
67
What indicators what make us check kidney function?
High BP Proteinuria Haematuria
68
Proteinuria and CKD together increase the risk of ...
Death by cardiovascular disease | More likely to need dialysis
69
What is the normal serum creatinine?
80 - 120 micromoles/L
70
What clearance markers can we use to represent eGFR?
Creatinine Inulin Cr EDTA Iohexol
71
What are the problems with using clearance markers to estimate GFR?
Expensive Require hospital stays Collecting urine has bad compliance
72
Is the relationship between serum creatinine and GFR linear?
No
73
How much of your renal function can you lose before serum creatinine will change?
~ 60%
74
Creatinine concentration in serum is determined by:
``` Renal function Muscle mass (age, sex, race, exercise) ```
75
Why can't we use eGFR in AKI?
Can only use the eGFR formula if GFR is relatively stable
76
What can we look for in blood to indicate the cause of CKD?
``` Autoantibody screen Complement Immunoglobulin ANCA CRP SPEP/UPEP ```
77
Describe polycystic kidneys
Autosomal dominant Can become very large Have CKD from the day they are born by definition but usually an issue until later in life
78
Acidosis can affect which organs?
Muscles Bones Renal function decline further
79
Acidosis is not a problem until GFR is ...
< 25
80
How does CKD lead to anaemia?
Decreased production of EPO Increased resistance to EPO (uraemic environment) Reduced RBC lifespan
81
How do we treat anaemia from CKD?
Give EPO subcutaneous injections
82
How can CKD cause mineral and bone disorders?
Decreased GFR leads to increased serum phosphate and decreased serum calcium Increased production of PTH Decreased active vitamin D - decreased Ca2+ gut absorption
83
What types of renal osteodystrophy can occur?
Rugger jersey spine - sclerosis of end plates Erosion to terminal phalanges Bone cysts
84
What are vertebral end plates?
The top and bottom portions of vertebral bodies that interface with vertebral discs
85
What other non-bone calcification can occur in CKD?
Aorta Shoulder joint Small vessels in skin
86
What can we do to help prevent/delay CKD?
``` Stop smoking Increased exercise Lose weight Treat diabetes Treat BP Treat proteinuria (ACEi) Lipid lowering ```
87
When is renal replacement therapy usually needed? (GFR)
GFR = 8 - 10 ml/min
88
What are the indications in CKD for dialysis?
``` Uraemic symptoms Acidosis Pericarditis Fluid overload Hyperkalaemia ```

Urinary System (14 decks)

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