renal Flashcards

(61 cards)

1
Q

nephrotic syndrome following recent EBV infection

-nothing seen on light microscopy of kidney
-electron microscopy shows fusion of podocytes

management?

A

Minimal change disease

1st= prednisolone
2nd= cylophosphamide

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2
Q

imageing of renal stones?

A

investigation
1st= non contrast CT KUB
pregnant/ child= US

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3
Q

management of renal stones?

A

Pain:
1st= NSAID (IM if admitted)

<5mm + asymptomatic
-watch + wait

5mm- 10mmm
-shockwave lithotripsy
Lithotripsy CI pregnancy- retrograde uretroscopy

10mm- 20mm
-shockwave lithotripsy OR nephrolithotomy
Lithotripsy CI pregnancy- retrograde uretroscopy

> 20mm
-nephrolithotomy

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3
Q

diagnosis of AKI?

A

Rise in creatinine:
>25 ml in 48 hours
OR
>= 50% rise in creatinine over 1 week
OR
< 0.5ml/kg/hour for more than 6 hours in adults

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3
Q

Stage 1 AKI?

A

Creatinine:
1.5- 1.9 x the baseline
OR
>26 mol rise

UO:
<0.5ml/kg/ hour in 6 hours

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4
Q

management of ureteric stones

A

Pain
1st= NSAID (IM if admission)

<10mm
alpha blockers + shockwave lithotripsy

10 - 20 mm
-retrograde uretoscopy

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4
Q

1st line imageing- prostate cancer

A

multi parametric MRI

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5
Q

Stage 2 AKI?

A

Creatinine:
2.0- 2.9 baseline

UO
<0.5ml/ kg/ hour over 12 hours

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6
Q

Stage 3 AKI?

A

Creatinine:
>3 x baseline
OR
>353.6
OR
Initiation of renal replacement
OR
Decrease in eGFR <35ml/min

UO
<0.3 ml/ kg/ hour for 24 hours
OR
Anuria

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7
Q

drugs that need stopped in AKI

A
  • NSAIDs (apart from cardioprotective aspirin)
  • Aminoglycosides
  • ACE inhibitors
  • Angiotensin II receptor antagonists
  • Diuretics
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8
Q

drugs that may have to be stopped in AKI as increased risk of toxicity (but doesn’t usually worsen AKI itself)

A
  • Metformin
  • Lithium
  • Digoxin
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9
Q

causes- pre renal AKI

A
  • Insufficient blood supply to kidneys reduces the filtration of blood
    • Dehydration- lack of intake, vomiting, diarrhoea, burns
    • Pre renal uraemia
    • Shock- sepsis, blood loss, anaphylaxis
    • Heart failure
    • Renal artery stenosis
    • NSAIDa/ COX-2
      ACEI/ ARBs
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10
Q

investigations AKI

A

-Creatinine
-U&E
-Urynalisis
-No identifiable cause for deterioration or are at risk of urinary tract obstruction= renal US within 24 hours

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11
Q

Patients at risk of AKI (e.g. on nephrotoxic drugs) requiring investigations with contrast

management

A

give fluid (reduces risk)

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12
Q

symptoms AKI

A

Many patients with early AKI may experience no symptoms. However, as renal failure progresses the following may be seen:

-reduced urine output
-pulmonary and peripheral oedema
-arrhythmias (secondary to changes in potassium and acid-base balance)
-features of uraemia (for example, pericarditis or encephalopathy)

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13
Q

causes- hyperkalaemia

A

-acute kidney injury
-drugs: ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin
-metabolic acidosis
-Addison’s disease
-rhabdomyolysis
-massive blood transfusion

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14
Q

management of mild hyperkalaemia

A

Mild (5.5 - 5.9 mmol/L)
Monitor potassium levels
Identify and address precipitating factors
Review and discontinue aggravating medications (e.g. ACE inhibitors)

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15
Q

management of moderate hyperkalaemia

A

Moderate (6.0 - 6.4 mmol/L)
Monitor ECG for changes
Consider IV calcium gluconate if ECG changes present
Administer insulin/dextrose infusion
Consider nebulised salbutamol
Address underlying causes and stop exacerbating drugs

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16
Q

management of severe hyperkalaemia

A

Severe (≥ 6.5 mmol/L) or ECG changes
Immediate treatment required
IV calcium gluconate to stabilise myocardium
Insulin/dextrose infusion for potassium shift
Nebulised salbutamol as adjunct therapy
Initiate potassium removal strategies (e.g. calcium resonium, loop diuretics, dialysis)

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17
Q

ECG changes hyperkalaemia

A

peaked or ‘tall-tented’ T waves (occurs first)
loss of P waves
broad QRS complexes
sinusoidal wave pattern

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18
Q

drugs causing AIN?

A

drugs: the most common cause, particularly antibiotics
-penicillin
-rifampicin
-NSAIDs
-allopurinol
-furosemide

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19
Q

apart from drugs- what are other causes of AIN?

A

systemic disease: SLE, sarcoidosis, and Sjogren’s syndrome
infection: Hanta virus , staphylococci

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20
Q

histology: marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules

+ AKI

what is the cause

A

AIN

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21
Q

specific features presentation + investigation AIN

A

some present + think they have had allergic reaction:
-flank pain
-arthalgia
-fever
-rash
-hypertension

urynalisis:
-white cell casts
-sterile pyuria

bloods: esosinophilia

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22
causes ATN
ischaemia: -shock -sepsis nephrotoxins: -aminoglycosides -myoglobin secondary to rhabdomyolysis -radiocontrast agents -lead
23
urynalisis ATN
muddy brown casts
24
what dose Use of 0.9% Sodium Chloride for fluid therapy in patients requiring large volumes risk?
hyperchloraemic metabolic acidosis
25
what med is recommended to all patients with CKD?
statin
26
when should someone with CKD start an ACEI?
ACR >30 + hypertension OR ACR> 70 no hypertension
27
electrolyte abnormalities tumour lysis syndrome
increase uric acid increase potassium increase phosphate decrease calcium
28
management tumour lysis syndrome
IV fluids during leukemia/ lymphoma chemo prophylactic: -Rasburicase OR -Allopurinal
29
what is HUS a triad of?
-AKI -Microangiopathic haemolytic anaemia (coombs -ve) -Thrombocytopenia
30
what can be seen on blood film HUS
schistocytes bloods film is most useful diagnostic test
31
managent HUS
fluids -no role for antibiotics
32
histology -IgA nephropathy
histology: mesangial hypercellularity, positive immunofluorescence for IgA & C3
33
diseases associated with IgA nephropathy
-Coeliac -alcoholic liver cirrhosis -henoch shonlein
34
management IgA nephropathy -isolated haemturia -no/ minimal protein -normal GFR
nothing -just monitor
35
management IgA nephropathy -persistent proteinuria -normal/ slightly reduced GFR
ACEI
36
management IgA nephropathy -not responding to ACEI -falling GFR
immunosupresion with steroids
37
is post streptococcal glomerulonephritis or IgA nephropathy associated with low complement?
post streptococcal glomerulonephritis
38
cause of Alports syndrome
X linked recessive -defect in type IV collagen (which makes up the lamina, the middle layer, of the GBM)
39
presentation alports syndrome
micropscopic haematuria -bilateral sensorineural hearing loss -retinitis pigmentosa -lenticonus
40
renal biopsy- Alports
splitting of the lamina densa- BASKET WEAVE APPEARANCE
41
what syndromes are strictly nephritic
-IgA nephropathy -Rapidly progressive glomerulonephritis -Alport's syndrome
42
management of henoch shonlein purpura
monitor renal function (urynalisis) + BP
43
what diseases cause rapidly progressive glomerulonephritis?
Goodpastures GPA / Wegeners Microscopic polyangitis SLE
44
histology rapidly progressive glomerulonephritis
glomerular crescents
45
management of rapidly progressive glomerulonephritis?
Management= immunosuppression (steroids + cyclophosphomide + azathioprine) +/- plasmapheresis (if haemorrhage) +/- temporary RRT
46
what fluid is given for fluid challenge?
No heart failure= 500 ml cystalloid (e.g. saline) stat Evidence of heart failure= 250 ml crystalloid (e.g. saline) stat
47
what has been shpwn to reduce the rate of CKD progression in ADPKD
tolvaptan
48
why are nephrotic patients hypercoagulable?
The patient is in a hypercoagulable state due to loss of antithrombin III and plasminogen via the kidneys
49
biopsy of post streptococcal glomerulonephritis?
sub epithelial humps (immune complex deposition) Immunoflourescence (starry sky) neurtrophils
50
what is seen membranoproliferative biopsy?
tram tracks
51
management membranoproliferative glomerulonephritis
ACEI STEROIDS +/- cyclosphamide
52
minimal change disease, what is seen on biopsy
-Normal glomeruli on light microscopy minimal change on microscopy -Fusion of podocytes and effacement of foot processes
53
minimal change nephritic or nephrotic?
nephrotic
54
minimal change treatment
1st= steroids 2nd= cyclophosphomide prophylactic LMWH
55
in renal transplant are cadaver or living donor grafts preferred
living Graft survival 1 year = 90%, 10 years = 60% for cadaveric transplants 1 year = 95%, 10 years = 70% for living-donor transplants
56
most commmon organism causing dyalisis peritonitis
Staph epidermis 2nd= staph aureus
57
medication for peritoneal dyalisis
vancomycin (or teicoplanin) + ceftazidime added to dialysis fluid OR vancomycin added to dialysis fluid + ciprofloxacin by mouth
58
what is the goal for iron replacement in CKD before EPO
transferrin sat ≥20% and ferritin ≥100 μg/L if not managed with oral iron in 3 months switch to IV