renal Flashcards

(38 cards)

1
Q

high urea after fall, likely cause of AKI

A

Prerenal disease - raised serum urea:creatinine ratio

dehydration

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2
Q

A 45-year-old man has recently been diagnosed with stage 5 chronic kidney disease (CKD) by a nephrologist. He started taking a new medication 6 weeks ago to treat symptoms that have developed because of his CKD. Over the last 3 weeks, he has developed abdominal pain, back pain, muscle weakness and is feeling quite anxious.

Which of the following medications would explain his symptoms?

A

calcium acetate - Patient with CKD taking calcium-based binders can have problems including hypercalcaemia and vascular calcification

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3
Q

An 8-year-old child is brought into the emergency department after having 5 episodes of bloody diarrhoea. Her parents say that the diarrhoea began 3 days ago after a barbecue at a friends house but it did not turn bloody until today. On examination, the child is pyrexial at 38 degrees with diffuse abdominal pain. Blood test are taken which show a thrombocytopenia, raised urea, creatinine and lactate dehydrogenase.

Which of the following organisms has most likely caused this infection?

A

haemolytic uraemic syndrome - e coli

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4
Q

cause of Aki if urine osmolality > 500 mOsm/kg

A

Prerenal disease - urine osmolality > 500 mOsm/kg

Prerenal disease is correct. Causes of acute kidney injury are broadly categorised as prerenal, renal or post-renal. Prerenal causes include anything that may lead to hypoperfusion of the kidney, such as dehydration, shock or haemorrhage. In a hypovolaemic state, whereby prerenal AKI can occur, the physiological response of the renal system is to retain salt and water in an effort to replenish the deplete circulatory volume. With this concept in mind, urine becomes concentrated (high osmolality) due to the reabsorption of water, and low in sodium, as the mechanism of fluid reabsorption relies on the retention of sodium. Further, prerenal AKI typically responds well to a fluid bolus as this is directly treating the underlying cause of the problem.

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5
Q

high urine protein to creatinine ratio, nothing on biopsy, URTI 2 days prior. cause of nephrotic syndrome?

A

This patient’s clinical presentation is consistent with minimal change disease, with the onset of nephrotic syndrome following a viral upper respiratory tract infection. In minimal change nephropathy, a kidney biopsy shows normal appearances on light microscopy and electron microscopy would demonstrate foot process effacement when available. The correct course of action is to commence prednisolone. The Kidney Disease: Improving Global Outcomes (KDIGO) guideline recommends starting prednisolone at 1 mg/kg daily unless contraindicated.

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6
Q

patients to fail to respond to erythropoietin therapy?

A

iron deficiency

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7
Q

if urea AND creatinine elevated

A

less likely to be upper GI bleed more likely to be CKD

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8
Q

pale and low Hb in CKD

A

CKD causing anaemia

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9
Q

episodes of visible haematuria that typically occur within a day or two of developing an upper respiratory tract infection.

cause of glomerulonephritis?

A

IgA nephropathy

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10
Q

Post strep GN presentation

A

1-3 weeks after their infection.

no raised eosinophils

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11
Q

fever, arthralgia, rash

raised WCC and eosinophils , AKI

cause?

A

Acute interstitial nephritis causes an ‘allergic’ type picture consisting usually of raised urinary WCC and eosinophils, alongside impaired renal function

triggered by penicillins

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12
Q

looking for aneurysm in AUPKD?

A

MRA head

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13
Q

IgA nephropathy presentation

A

2-3 days post URTI, macroscopic haematuria

IgA and C3 deposits in sub-endothelium

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14
Q

systemic steroids can cause

A

avascular necrosis

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15
Q

anti GBM and ANCA positive ?

A

Anti GBM disease (rapidly progressive glomerulonephritis) - corticosteroids and plasmophoresis

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16
Q

renal papillary necrosis due to naproxen mx?

A

urgent drainage

17
Q

post strep GN biopsy

A

sub epithelial humps in glomeruli

18
Q

minimal change disease on biopsy

A

podocyte damage on electron

19
Q

HTN and high renin cause of refractory HTN?

A

renal artery stenosis

Primary and secondary aldosteronism can be differentiated by looking at the renin levels. If renin is high then a secondary cause is more likely, i.e renal artery stenosis.

20
Q

ADPKD physical exam finding

A

mitral valve disease and hepatomegaly

Extra-renal features of ADPKD include:
Hepatic cysts which manifest as hepatomegaly
Diverticulosis
Intracranial aneurysms
Ovarian cysts

21
Q

indication that kidney disease is chronic not acute

A

low calcium

high phosphate can be seen in either q

22
Q

Prolonged diarrhoea may result in a

A

metabolic acidosis associated with hypokalaemia

23
Q

what can invalidate eGFR

A

Eating red meat the evening before a blood test can invalidate eGFR result

24
Q

anaemia in CKD order of management

A

Anaemia in CKD: correct iron deficiency before starting erythropoiesis-stimulating agents

25
treatment for VTE prophylaxis if albumin is 19 (normal 35-50)
Increased risk of VTE in patients with nephrotic syndrome - prophylactic LMWH required aspirin if 25-32 albumin
26
A 69-year-old woman with a history of well-controlled temporal arteritis presents to the emergency department following a collapse at home, and is complaining of severe persisting abdominal pain. Her husband reports that she has been following her daily steroid regime, and that she has recently been recovering from 'a nasty bout of flu'. Initial observations and examination identify a low-grade fever and generalised abdominal tenderness, with a GCS of 13/15. Which of the following acid-base imbalances would be most expected in this patient, given the likely underlying pathology?
Addison's disease/adrenal insufficiency can cause hyperkalaemic metabolic acidosis
27
Use of 0.9% Sodium Chloride for fluid therapy in patients requiring large volumes =
risk of hyperchloraemic metabolic acidosis
28
alports features
Alport's syndrome is a genetic disorder characterized by glomerulonephritis, end-stage kidney disease, and hearing loss. It can also affect the eyes, leading to abnormalities such as lenticonus. However, it does not cause anosmia or loss of smell.
29
Pulmonary oedema is an indication for
haemodialysis in a patient with acute kidney injury
30
unknown AKI Ix
An ultrasound is required in the investigation of all patients presenting with an AKI of unknown aetiology
31
AKI diagnostic test results
NICE recognise any of the following criteria to diagnose AKI in adults: ↑ creatinine > 26µmol/L in 48 hours ↑ creatinine > 50% in 7 days ↓ urine output < 0.5ml/kg/hr for more than 6 hours can still have raised CRP (doesn't mean its UTI)
32
USS kidney size in chronic diabetic nephropathy vs CKD
Chronic diabetic nephropathy will have large/normal sized kidneys on ultrasound whereas most patients with chronic kidney disease have bilateral small kidneys
33
ABG showing metabolic acidosis, way to find cause
The anion gap is calculated by calculating the difference between positively charged ions (sodium and potassium) and negatively charged ions (bicarbonate and chloride). In this case (143 + 5) - (17 + 100) gives an anion gap of 31 mmol/L. A normal anion gap is 8-14 mmol/L. This patient, therefore, has metabolic acidosis with a raised anion gap. Raised anion gap shows there is excess acid in the blood. The only listed cause of raised anion gap metabolic acidosis is septic shock, which results in acidosis due to the production of lactic acid due to inadequate tissue perfusion.
34
anion gap
(sodium and potassium) - (bicarbonate and chloride) normal is 8-14 high = could be sepsis
35
4+ proteinuria on urine dipstick, hypoalbuminemia (serum albumin of 20 g/L), and pitting oedema, which are classic signs of x The presence of periorbital oedema, fatigue, and foamy urine further supports this diagnosis.
Nephrotic syndrome is associated with an increased risk of thrombosis, which explains the left leg pain, erythema, swelling, and elevated D-dimer consistent with deep vein thrombosis (DVT). This is because there is a loss of antithrombin III, protein C, and protein S, with an associated rise in fibrinogen levels, predisposing to thrombosis. Such patients should be offered prophylactic low molecular weight heparin to reduce the risk of thrombosis.
36
nephrotic syndrome reason for increased VTE
Loss of antithrombin III
37
initial mx of pt with raised K+ 6.1
12 lead ECG The British National Formulary (BNF) management of hyperkalaemia is as follows: If K+ > 6.5 mmol/l or if there are ECG changes: Administer calcium gluconate 10% 10-20ml by slow IV injection titrated to ECG response Give 10 U Actrapid in 50 ml of 50% glucose over 10-15 minutes Consider use of nebulised salbutamol Consider correcting acidosis with sodium bicarbonate infusion Management of hyperkalaemia, BNF, June 2016 Given that the patient's K+ is only 6.1 at the moment, an ECG would be the first thing to do. It would also be sensible to repeat the K+ reading, probably with a venous blood gas but an ECG would reveal whether there was an immediate danger which needs treatment.
38