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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
Give some examples of endogenous nephrotoxins.
Myoglobin Urate Bilirubin
26
Give some examples of endogenous nephrotoxins which cane lead to ATN.
``` Endotoxin X-Ray contrast Drugs: ACEI, Aminoglycosides, NSAIDs Weed killers Antifreeze ```
27
How can sepsis cause ATN?
Exact mechanism is unknown but it combines ischaemia with endotoxin damage
28
How can urine biochemistry be used to differentiate between pre-renal and ATN AKI?
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
29
Why can urine biochemistry not exclusively be used to diagnose pre-renal vs ATN AKI?
Other factors affect the ability to concentrate urine e.g. age
30
What type of AKI do glomerular and arteriolar disease cause?
Intrinsic
31
What is primary acute glomerulonephritis?
Where disease only affects the kidneys e.g. IgA nephropathy
32
How does secondary glomerulonephritis differ from primary?
Kidneys are involved as part of systemic process e.g. SLE, vasculitis
33
How does granulomatosis with polyangitis (Wegener's granulomatosis) cause intrinsic AKI?
Walls of BV become inflamed --> rapidly progressive crescenting necrotising glomerulonephritis
34
What can lead to microangiopathic haemolytic anaemia causing intrinsic AKI?
Haemolytic uraemia syndrome Malignant hypertension Pre-eclampsia
35
What is the pathogensis of microangiopathic haemolytic anaemia?
Endothelial damage --> platelet thrombi --> partial occlusion of small arteries --> RBC destruction
36
What type of AKI can acute tubulo-interstitial nephritis lead to?
Intrinsic
37
What happens in acute tubulo-interstitial nephritis due to infection?
Acute pyelonephritis leads to increased spacing of functional tubules due to inflammatory cell infiltration, esp eosinophils
38
What are the common causes of toxin induced acute tubulo-interstitial nephritis leading to interstitial AKI?
Abx, NSAIDs, PPIs | In high-risk pts consider all drugs until prove otherwise
39
What proportion of AKI cases are due to obstructive AKI?
5-10%
40
On which population is obstructive AKI more common?
Elderly
41
Why must the obstruction in obstructive AKI block both kidneys or a single functioning kidney?
It is possible to survive on one kidney with the only detectable change being a slight increase in creatinine
42
What is the pathogenesis of obstructive AKI?
Obstruction with continuous urine production --> increased intraluminal pressure --> dilation of renal pelvis --> decrease in renal function
43
What is hydronephrosis?
Dilation of renal pelvis
44
Give some examples of intraluminal causes of obstructive AKI.
Stones, blood clots or tumour within kidney, ureter or bladder
45
What criteria must renal stones have to fit in order to cause obstructive AKI?
Be in both renal pelvises or ureters or be obstruction neck of bladder/urethra >10 mm
46
Why will renal stones in the kidney tissue not lead to obstructive AKI?
Too small
47
What within-wall causes can lead to obstructive AKI, although tend to lead to CKD instead?
Congenital megaureter | Post-TB stricture
48
What causes from pressure outside can lead to obstructive AKI?
Enlarged prostate Cervical/uterine tumour Aortic aneurysm Ligation of ureter during surgery
49
What four-step approach should be used for a pt with AKI?
Regulate BP and blood volume Regulate pH, electrolytes and osmolarity Excretion of waste inc metabolism of drugs Endocrine function of kidney
50
How will a pt with AKI who is volume depleted present on examination?
``` Cool peripheries Fast pulse Low BP/postural hypotension Reduced JVP Decreased skin turgor Dry axillae ```
51
How will a pt with AKI who is volume overloaded present on examination?
Gallop rhythm Increased JVP Pulmonary oedema Peripheral oedema (sacral/ankle)
52
How will a pt with AKI and sepsis present O/E?
``` Pyrexia Rigors Warm peripheries Bounding pulse Rapid capillary refill Hypotension ```
53
How will a pt with AKI and urinary tract obstruction present O/E?
``` 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
What must every pt with AKI have?
Urinalysis for blood, protein and leukocytes
55
What do grossly elevated levels of blood and protein on dipstick analysis in AKI indicate?
Intrinsic renal AKI
56
How will pre-renal AKI appear on investigation?
No proteinuria or haematuria and normal microscopy
57
How will glomerulonephritis present on investigation in AKI?
+++ proteinuria +++ haematuria RBC casts on microscopy
58
Does ATN cause proteinuria and/or haematuria?
No
59
Is microscopy performed for ATN in AKI?
No
60
What is Rhine biochemistry used to investigate in AKI?
Osmolality and urine sodium in cases where electrolytes are severely deranged to see if this is due to the kidneys
61
When is an US scan performed within 24 hrs of presentation in AKI?
Suspected obstructive AKI | If pre-renal of ATN AKI doesn't respond to Tx
62
Why might a CXR be used to investigate AKI?
Identifies fluid overload +/- infection
63
When is a kidney biopsy performed to investigate AKI?
Pre- and post renal AKI have been ruled out + Confident diagnosis of ATN cannot be made + Systemic inflammation
64
What are the risk factors for developing AKI?
``` Increasing age CKD Heart disease Liver disease DM Cancer Neurological impairment Previous AKI Dehydration Sepsis Burns Trauma Radio-iodinated contrast in last week ```
65
Why is liver disease a risk factor for AKI?
Poor blood supply to kidney | Nephrotoxic bilirubin to kidney
66
How can AKI be prevented?
Monitor 'at risk' pts closely, esp when prescribing Ensure adequate hydration Avoid nephrotoxins Early detection and cause identification
67
How is volume overload in AKI managed?
Restrict dietary sodium and water intake to
68
How is hyperkalaemia in AKI managed?
``` 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
What is the effect of using beta-2 agonists to treat hyperkalaemia in AKI?
Transiently drives K+ into cells
70
How is acidosis in AKI managed?
Restrict protein in diet (watch out for malnutrition) | NaHCO3-
71
When is dialysis used to manage AKI?
``` Hyperkalaemia after Tx Metabolic acidosis where NaHCO3- inappropriate Fluid overload after diuretics Presence of dialysable nephrotoxin Signs of uraemia ```
72
Give examples of dialysable nephrotoxins which would indicate management of AKI with dialysis irrespective of disease stage.
Aspirin | Ethylene glycol
73
What are the signs of uraemia?
Pericarditis Decreased GCS Intractable N&V
74
What are the outcomes following AKI?
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
Why does any disease that affects the vasculature of the glomerulus have a downstream affect on the associated tubule?
It receives its blood supply from the efferent arteriole or the glomerulus
76
What are the functions of the kidney?
Excretion: water, salt, electrolytes, acid, metabolic waste Glomerular permselecitivty Tubular: [urine], HCO3- reabsorption, NH4+ secretion Endocrine: 1-alpha-calcidiol, renin, erythropoietin
77
Does a pt presenting with pain indicate glomerulonephritis of diabetic nephropathy?
No these are painless. Indicates stones or back pain
78
Can urinary appearance be used to identify renal disease?
No, too variable
79
Does urinary flow disturbance indicate renal disease?
No, often due to urological disturbance
80
What are the sequelae of impaired kidney excretion?
``` Hyperkalaemia Sodium and water overload Acidosis Metabolic waste products in blood Uraemia syndrome ```
81
What died the rate of excretion by the kidney depend on?
Rate of filtration
82
What are the sequlae of impaired glomerular permselectivity?
Proteinuria | Haematuria
83
What is the earliest indication of kidney disease?
Impaired urine concentrating ability leading to frequency and nocturia
84
What can impaired tubular function in kidney diseases contribute to?
Acidosis
85
Why is glycosuria seen with normal blood glucose in impaired tubular functions?
Renal glucose threshold is lowered
86
How can the effect of impaired tubular function on renal glucose threshold be used to Tx DM?
SGLT2 inhibitor causes lowering of renal glucose threshold so more is lost in the urine
87
What are the sequelae of impaired endocrine function of the kidneys in renal disease?
Vitamin D not activated --> metabolic bone disease Decreased erythropoietin --> renal anaemia Decreased renin --> hypertension
88
What do the S/S of renal disease depend on?
Speed of onset
89
Which pts are routinely scanned for kidney disease due to asymptomatic nature?
``` Hypertensive Heart disease DM Urinary tract obstruction Systemic disease e.g. Myeloma or lupus ```
90
What is the most common cause of microscopic haematuria?
UTI
91
Give some examples of causes of microscopic haematuria.
``` Polycystic kidneys Renal stones Tumours Arteriovenous malformations Kidney/glomerular disease ```
92
What do pts >45 y.o. require as primary investigation following detection of microscopic haematuria?
Cystoscopy
93
How does blood form the top of the glomerular pathway present in macroscopically haematuria?
Red urine throughout stream
94
If blood in macroscopic haematuria clots, where is it likely to be from?
Bladder or tumour, not glomerulus
95
Where is blood at the beginning or end of stream likely to be from?
Ureters or bladder
96
What does macroscopic haematuria need to be distinguished from?
Haemoglobinuria Myoglobinuria Food dyes
97
What is the most common cause of glomerular haematuria?
IgA nephropathy within 24 hours of URTI
98
Is glomerular haematuria painful?
No usually painless
99
What might be seen on investigation of glomerular haematuria and why?
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
Is Tomm-Horsfall microprotein secretion by tubular cells always pathological?
Yes
101
How does proteinuria present?
Frothy urine
102
What are the sequelae of significant amounts of protein loss via the urine?
Oedema due to albumin loss Infection due to immunoglobulin loss Prothrombotic state due to coagulation cascade protein loss
103
What is the classic triad of findings in nephrotic syndrome?
Proteinuria which is significant enough to cause hypoalbuminaemia and oedema
104
What additional finding is seen in nephrotic syndrome as well as the classic triad?
Hyperlipidaemia due to liver function disturbance
105
What is the classic triad of nephrotic syndrome pathognomonic of?
Glomerular disease needing renal biopsy to determine cause
106
What is the cause of all nephrotic syndrome presentations?
Disruption of fort processes of podocytes in the glomerular permselectivity membrane
107
What is the clinical presentation of a pt with nephrotic syndrome?
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
What is classic nephritic syndrome?
Post-streptococcal glomerulonephritis in children
109
Why is classic nephritic syndrome not now commonly seen in the UK?
Abx
110
What are the S/S of rapid onset nephritic syndrome?
``` Oliguria Hypertension General oedema Haematuria Normal serum albumin Variable renal impairment Urine with blood, protein and cell casts ```
111
What is needed to diagnose nephritic syndrome?
Biopsy to identify different ultra structural damage to nephrotic syndrome
112
How does nephritic syndrome compare to nephrotic syndrome?
Faster onset, less oedema, raised BP, raised JVP, less proteinuria, more haematuria, red cell casts are present and serum albumin is NOT lowered
113
What is rapidly progressive glomerulonephritis?
Clinical situation where severe glomerular injury different to nephrotic and nephritic injury causes decreased renal function over days
114
How might a pt with rapidly progressive glomerulonephritis present?
Uraemia emergency with evidence of extra-renal disease due to systemic cause
115
What is rapidly progressive glomerulonephritis associated with?
Crescentic glomerulonephritis Anti neutrophil cytoplasmic antibodies Anti glomerular BM antibodies Systemic vasculitis
116
On what imaging is systemic vasculitis visible?
CXR | CT scan
117
What is the commonest cause of kidney disease?
CKD
118
Describe the progression of CKD?
Slow, pts don't present until GFR sob, N+V, aches+pains, sleep reversal, nocturia, restless legs, itching, chest pains --> seizures and coma

Semester 3 (50 decks)

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