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Semester 3 > Urinary Session 9 > Flashcards

Urinary Session 9 Flashcards

1
Q

Why is acute kidney injury hard to define using measured levels?

A

Actual GFR fluctuates normally but is largely constant whereas the creatinine peak used for staging isn’t detectable until 7 days after insult

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2
Q

Why is AKI a medical emergency?

A

Rapidly leads to renal failure

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3
Q

How does serum creatinine change through stages 1-3 of AKI?

A 
1= 150-200% increase from baseline
2= >200-300% increases
3= >300 %
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4
Q

What causes the majority of AKI cases in the UK?

A

85% prerenal or ATN

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5
Q

What are common causes of AKI seen outside of the UK?

A

Infection
Diarrhoeal illness
Obstetric
Occupational e.g. Copper sulphate in the dye industry

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6
Q

What is acute kidney injury?

A

A clinical syndrome caused by an abrupt decreases in actual GFR which can be over days to weeks leading to upset of ECF volume, electrolyte and acid/base disturbance and accumulation of nitrogenous waste

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7
Q

What is the pathogenesis of pre-renal AKI?

A

Actual GFR decreases due to decreased renal blood flow

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8
Q

Why can the kidneys respond to pre-renal AKI and not some other types?

A

No cell damage

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9
Q

How does the kidney respond to pre-renal AKI?

A

Avid reabsorption of sodium and water via aldosterone and ADH release

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10
Q

What medications can lead to pre-renal AKI?

A

NSAIDs

ACEI/ARBs

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11
Q

How can NSAIDs cause pre-renal AKI?

A

Switch off prostaglandin synthesis therefore decreased afferent vasodilation and subsequent decrease in actual GFR

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12
Q

How can ACEI/ARBs cause pre-renal AKI?

A

Decrease circulating vasoconstrictors causing a decrease in actual GFR

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13
Q

How can DM lead to pre-renal AKI?

A

Causes disease of afferent arteriole –> hypersensitivity or insensitivity to stimuli so GFR cannot be maintained

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14
Q

What causes of decreased ECV can lead to pre-renal AKI?

A

Hypovolaemia due to blood/fluid loss or 3rd spacing
Cardiac failure due to LV dysfunction, valve disease or tamponade
Systemic vasodilation due to sepsis, cirrhosis or anaphylaxis

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15
Q

What dual action can sepsis have to contribute towards development of pre-renal AKI?

A

Causes systemic vasodilation and vasodilation of the efferent arteriole

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16
Q

What disease states can lead to impaired renal autoregulation leading to pre-renal AKI?

A

Pre glomerular vasoconstriction due to sepsis, hypercalcaemia, hepatorenal syndrome, NSAID Tx
Post glomerular vasodilation due to ACEI or ARBs

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17
Q

What is acute tubular necrosis?

A

When PCT cells are damaged and need replacing and are therefore not reabsorbing sodium or managing water levels effectively

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18
Q

Which cells are implicated in acute tubular necrosis and why?

A

PCT as they are most vulnerable due to their high energy demands

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19
Q

Why should aggressive fluid resuscitation not be used to treat acute tubular necrosis?

A

Damaged PCT cells cannot expel excess water so would lead to overload

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20
Q

Which blood vessels are implicated in ischaemia leading to ATN?

A

Peritubular capillaries

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21
Q

Why are the PCT and thick ascending limb of Henle’s loop at risk of damage from ischaemia?

A

Outer medulla is relatively hypoxic due to BV distribution

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22
Q

In ATN due to ischaemia, why are the glomerulus and distal tubules preserved?

A

Glomerulus receives sufficient bloody supply and the distal tubules have lower oxygen demands so also receive sufficient blood supply

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23
Q

How do nephrotoxins cause ATN?

A

Damage tubule-lining epithelial cells –> cell death and shedding into lumen

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24
Q

When is nephrotoxin damage much more likely to lead to ATN?

A

During reduced perfusion

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25
Q

Give some examples of endogenous nephrotoxins.

A

Myoglobin
Urate
Bilirubin

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26
Q

Give some examples of endogenous nephrotoxins which cane lead to ATN.

A 
Endotoxin
X-Ray contrast
Drugs: ACEI, Aminoglycosides, NSAIDs
Weed killers
Antifreeze
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27
Q

How can sepsis cause ATN?

A

Exact mechanism is unknown but it combines ischaemia with endotoxin damage

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28
Q

How can urine biochemistry be used to differentiate between pre-renal and ATN AKI?

A

Pre renal: specific gravity is raised, osmolality is raised, urinary sodium is low
ATN: specific gravity is reduced, osmolality is reduced, urinary sodium is raised

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29
Q

Why can urine biochemistry not exclusively be used to diagnose pre-renal vs ATN AKI?

A

Other factors affect the ability to concentrate urine e.g. age

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30
Q

What type of AKI do glomerular and arteriolar disease cause?

A

Intrinsic

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31
Q

What is primary acute glomerulonephritis?

A

Where disease only affects the kidneys e.g. IgA nephropathy

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32
Q

How does secondary glomerulonephritis differ from primary?

A

Kidneys are involved as part of systemic process e.g. SLE, vasculitis

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33
Q

How does granulomatosis with polyangitis (Wegener’s granulomatosis) cause intrinsic AKI?

A

Walls of BV become inflamed –> rapidly progressive crescenting necrotising glomerulonephritis

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34
Q

What can lead to microangiopathic haemolytic anaemia causing intrinsic AKI?

A

Haemolytic uraemia syndrome
Malignant hypertension
Pre-eclampsia

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35
Q

What is the pathogensis of microangiopathic haemolytic anaemia?

A

Endothelial damage –> platelet thrombi –> partial occlusion of small arteries –> RBC destruction

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36
Q

What type of AKI can acute tubulo-interstitial nephritis lead to?

A

Intrinsic

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37
Q

What happens in acute tubulo-interstitial nephritis due to infection?

A

Acute pyelonephritis leads to increased spacing of functional tubules due to inflammatory cell infiltration, esp eosinophils

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38
Q

What are the common causes of toxin induced acute tubulo-interstitial nephritis leading to interstitial AKI?

A

Abx, NSAIDs, PPIs

In high-risk pts consider all drugs until prove otherwise

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39
Q

What proportion of AKI cases are due to obstructive AKI?

A

5-10%

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40
Q

On which population is obstructive AKI more common?

A

Elderly

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41
Q

Why must the obstruction in obstructive AKI block both kidneys or a single functioning kidney?

A

It is possible to survive on one kidney with the only detectable change being a slight increase in creatinine

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42
Q

What is the pathogenesis of obstructive AKI?

A

Obstruction with continuous urine production –> increased intraluminal pressure –> dilation of renal pelvis –> decrease in renal function

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43
Q

What is hydronephrosis?

A

Dilation of renal pelvis

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44
Q

Give some examples of intraluminal causes of obstructive AKI.

A

Stones, blood clots or tumour within kidney, ureter or bladder

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45
Q

What criteria must renal stones have to fit in order to cause obstructive AKI?

A

Be in both renal pelvises or ureters or be obstruction neck of bladder/urethra
>10 mm

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46
Q

Why will renal stones in the kidney tissue not lead to obstructive AKI?

A

Too small

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47
Q

What within-wall causes can lead to obstructive AKI, although tend to lead to CKD instead?

A

Congenital megaureter

Post-TB stricture

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48
Q

What causes from pressure outside can lead to obstructive AKI?

A

Enlarged prostate
Cervical/uterine tumour
Aortic aneurysm
Ligation of ureter during surgery

49
Q

What four-step approach should be used for a pt with AKI?

A

Regulate BP and blood volume
Regulate pH, electrolytes and osmolarity
Excretion of waste inc metabolism of drugs
Endocrine function of kidney

50
Q

How will a pt with AKI who is volume depleted present on examination?

A 
Cool peripheries
Fast pulse
Low BP/postural hypotension
Reduced JVP
Decreased skin turgor
Dry axillae
51
Q

How will a pt with AKI who is volume overloaded present on examination?

A

Gallop rhythm
Increased JVP
Pulmonary oedema
Peripheral oedema (sacral/ankle)

52
Q

How will a pt with AKI and sepsis present O/E?

A 
Pyrexia
Rigors
Warm peripheries
Bounding pulse
Rapid capillary refill
Hypotension
53
Q

How will a pt with AKI and urinary tract obstruction present O/E?

A 
Anuria
Single functioning kidney
Loin/suprapubic pain
Hx of renal stones, prostatism, previous pelvic or abdominal surgery
Palpable bladder
Pelvic/abdominal mass
Enlarged prostate
Blocked catheter
54
Q

What must every pt with AKI have?

A

Urinalysis for blood, protein and leukocytes

55
Q

What do grossly elevated levels of blood and protein on dipstick analysis in AKI indicate?

A

Intrinsic renal AKI

56
Q

How will pre-renal AKI appear on investigation?

A

No proteinuria or haematuria and normal microscopy

57
Q

How will glomerulonephritis present on investigation in AKI?

A

+++ proteinuria
+++ haematuria
RBC casts on microscopy

58
Q

Does ATN cause proteinuria and/or haematuria?

A

No

59
Q

Is microscopy performed for ATN in AKI?

A

No

60
Q

What is Rhine biochemistry used to investigate in AKI?

A

Osmolality and urine sodium in cases where electrolytes are severely deranged to see if this is due to the kidneys

61
Q

When is an US scan performed within 24 hrs of presentation in AKI?

A

Suspected obstructive AKI

If pre-renal of ATN AKI doesn’t respond to Tx

62
Q

Why might a CXR be used to investigate AKI?

A

Identifies fluid overload +/- infection

63
Q

When is a kidney biopsy performed to investigate AKI?

A

Pre- and post renal AKI have been ruled out
+ Confident diagnosis of ATN cannot be made
+ Systemic inflammation

64
Q

What are the risk factors for developing AKI?

A 
Increasing age
CKD
Heart disease
Liver disease
DM
Cancer
Neurological impairment
Previous AKI
Dehydration
Sepsis
Burns
Trauma
Radio-iodinated contrast in last week
65
Q

Why is liver disease a risk factor for AKI?

A

Poor blood supply to kidney

Nephrotoxic bilirubin to kidney

66
Q

How can AKI be prevented?

A

Monitor ‘at risk’ pts closely, esp when prescribing
Ensure adequate hydration
Avoid nephrotoxins
Early detection and cause identification

67
Q

How is volume overload in AKI managed?

A

Restrict dietary sodium and water intake to

68
Q

How is hyperkalaemia in AKI managed?

A 
Immediately: calcium gluconate
Then:
Restrict dietary intake
Stop K+ sparing diuretics, ACEI and ARB
Exchange resins
Dextrose and insulin
NaHCO3- if HCO3- low
Beta-2 agonists
69
Q

What is the effect of using beta-2 agonists to treat hyperkalaemia in AKI?

A

Transiently drives K+ into cells

70
Q

How is acidosis in AKI managed?

A

Restrict protein in diet (watch out for malnutrition)

NaHCO3-

71
Q

When is dialysis used to manage AKI?

A 
Hyperkalaemia after Tx
Metabolic acidosis where NaHCO3- inappropriate
Fluid overload after diuretics
Presence of dialysable nephrotoxin
Signs of uraemia
72
Q

Give examples of dialysable nephrotoxins which would indicate management of AKI with dialysis irrespective of disease stage.

A

Aspirin

Ethylene glycol

73
Q

What are the signs of uraemia?

A

Pericarditis
Decreased GCS
Intractable N&V

74
Q

What are the outcomes following AKI?

A

Uncomplicated ATN –> 2-3wk recovery if no further insults
Uncomplicated ATN with hypotension on dialysis –> more ischaemic lesions –> prolonged recovery
Increased risk of death for one year following
Increased risk of CKD

75
Q

Why does any disease that affects the vasculature of the glomerulus have a downstream affect on the associated tubule?

A

It receives its blood supply from the efferent arteriole or the glomerulus

76
Q

What are the functions of the kidney?

A

Excretion: water, salt, electrolytes, acid, metabolic waste
Glomerular permselecitivty
Tubular: [urine], HCO3- reabsorption, NH4+ secretion
Endocrine: 1-alpha-calcidiol, renin, erythropoietin

77
Q

Does a pt presenting with pain indicate glomerulonephritis of diabetic nephropathy?

A

No these are painless. Indicates stones or back pain

78
Q

Can urinary appearance be used to identify renal disease?

A

No, too variable

79
Q

Does urinary flow disturbance indicate renal disease?

A

No, often due to urological disturbance

80
Q

What are the sequelae of impaired kidney excretion?

A 
Hyperkalaemia
Sodium and water overload
Acidosis
Metabolic waste products in blood
Uraemia syndrome
81
Q

What died the rate of excretion by the kidney depend on?

A

Rate of filtration

82
Q

What are the sequlae of impaired glomerular permselectivity?

A

Proteinuria

Haematuria

83
Q

What is the earliest indication of kidney disease?

A

Impaired urine concentrating ability leading to frequency and nocturia

84
Q

What can impaired tubular function in kidney diseases contribute to?

A

Acidosis

85
Q

Why is glycosuria seen with normal blood glucose in impaired tubular functions?

A

Renal glucose threshold is lowered

86
Q

How can the effect of impaired tubular function on renal glucose threshold be used to Tx DM?

A

SGLT2 inhibitor causes lowering of renal glucose threshold so more is lost in the urine

87
Q

What are the sequelae of impaired endocrine function of the kidneys in renal disease?

A

Vitamin D not activated –> metabolic bone disease
Decreased erythropoietin –> renal anaemia
Decreased renin –> hypertension

88
Q

What do the S/S of renal disease depend on?

A

Speed of onset

89
Q

Which pts are routinely scanned for kidney disease due to asymptomatic nature?

A 
Hypertensive
Heart disease
DM
Urinary tract obstruction
Systemic disease e.g. Myeloma or lupus
90
Q

What is the most common cause of microscopic haematuria?

A

UTI

91
Q

Give some examples of causes of microscopic haematuria.

A 
Polycystic kidneys
Renal stones
Tumours
Arteriovenous malformations
Kidney/glomerular disease
92
Q

What do pts >45 y.o. require as primary investigation following detection of microscopic haematuria?

A

Cystoscopy

93
Q

How does blood form the top of the glomerular pathway present in macroscopically haematuria?

A

Red urine throughout stream

94
Q

If blood in macroscopic haematuria clots, where is it likely to be from?

A

Bladder or tumour, not glomerulus

95
Q

Where is blood at the beginning or end of stream likely to be from?

A

Ureters or bladder

96
Q

What does macroscopic haematuria need to be distinguished from?

A

Haemoglobinuria
Myoglobinuria
Food dyes

97
Q

What is the most common cause of glomerular haematuria?

A

IgA nephropathy within 24 hours of URTI

98
Q

Is glomerular haematuria painful?

A

No usually painless

99
Q

What might be seen on investigation of glomerular haematuria and why?

A

Dysmorphic RBCs due to squeezing through glomerulus
Red cell cast as decreased flow/increased [salt]/decreased pH favour Tomm-Horsfall microprotein secretion by renal tubule cells

100
Q

Is Tomm-Horsfall microprotein secretion by tubular cells always pathological?

A

Yes

101
Q

How does proteinuria present?

A

Frothy urine

102
Q

What are the sequelae of significant amounts of protein loss via the urine?

A

Oedema due to albumin loss
Infection due to immunoglobulin loss
Prothrombotic state due to coagulation cascade protein loss

103
Q

What is the classic triad of findings in nephrotic syndrome?

A

Proteinuria which is significant enough to cause hypoalbuminaemia and oedema

104
Q

What additional finding is seen in nephrotic syndrome as well as the classic triad?

A

Hyperlipidaemia due to liver function disturbance

105
Q

What is the classic triad of nephrotic syndrome pathognomonic of?

A

Glomerular disease needing renal biopsy to determine cause

106
Q

What is the cause of all nephrotic syndrome presentations?

A

Disruption of fort processes of podocytes in the glomerular permselectivity membrane

107
Q

What is the clinical presentation of a pt with nephrotic syndrome?

A

Swelling around face (but able to lay flat)
Horizontal crescents on fingernails (Muehrcke’s bands)
Xanthelasma
Fat bodies in urine
Unilateral swollen leg due to oedema and DVT

108
Q

What is classic nephritic syndrome?

A

Post-streptococcal glomerulonephritis in children

109
Q

Why is classic nephritic syndrome not now commonly seen in the UK?

A

Abx

110
Q

What are the S/S of rapid onset nephritic syndrome?

A 
Oliguria
Hypertension
General oedema
Haematuria
Normal serum albumin
Variable renal impairment
Urine with blood, protein and cell casts
111
Q

What is needed to diagnose nephritic syndrome?

A

Biopsy to identify different ultra structural damage to nephrotic syndrome

112
Q

How does nephritic syndrome compare to nephrotic syndrome?

A

Faster onset, less oedema, raised BP, raised JVP, less proteinuria, more haematuria, red cell casts are present and serum albumin is NOT lowered

113
Q

What is rapidly progressive glomerulonephritis?

A

Clinical situation where severe glomerular injury different to nephrotic and nephritic injury causes decreased renal function over days

114
Q

How might a pt with rapidly progressive glomerulonephritis present?

A

Uraemia emergency with evidence of extra-renal disease due to systemic cause

115
Q

What is rapidly progressive glomerulonephritis associated with?

A

Crescentic glomerulonephritis
Anti neutrophil cytoplasmic antibodies
Anti glomerular BM antibodies
Systemic vasculitis

116
Q

On what imaging is systemic vasculitis visible?

A

CXR

CT scan

117
Q

What is the commonest cause of kidney disease?

A

CKD

118
Q

Describe the progression of CKD?

A

Slow, pts don’t present until GFR sob, N+V, aches+pains, sleep reversal, nocturia, restless legs, itching, chest pains –> seizures and coma

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