Renal Medicine Flashcards

1
Q

Define AKI and what determines diagnosis?

A

A sudden decline in renal function significant to produce uraemia and often oliguria (500umol/L

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2
Q

Normal U&E levels

A
Na : 135-145 mmol/L
K : 3.5-5 mmol/L
Creatinine : 70-150 umol/L
Urea : 2.5-6.7 mmol/L
eGFR : >90
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3
Q

RIFLE criteria

A

RISK - SCr raised 1.5/2 x baseline or GFR decreased >25%. Also urine output

INJURY - SCr raised 2/3 x baseline or GFR decreased >50%. Also urine output 3 x baseline or GFR decreased >75%. Also urine output 4 weeks therefore requiring dialysis

ESRF - failure >3 months. Dialysis required

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4
Q

Nephrotoxic Drugs

A

Diuretics
NSAIDS (dilate efferent arteriole)
ACEi (dilation of efferent & afferent)
(commonest)

All cause pre-renal failure with NSAIDS also causing ATN.

Aminoglycosides 
Cephalosporins 
Cocaine 
Lithium
Penicillins 
Valporate
(less common)
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5
Q

How do you assess fluid status?

A

Clinically -

BP (esp postural)
Oedema 
JVP
Peripheral perfusion (cap. refill)
Pulse 
Basal crackles (pulmonary oedema)
(*most useful*)

Skin turgor
Sunken eyes
Mucous membranes
(less useful)

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6
Q

Define nephrotic syndrome

A

Hypoalbuminaemia
Oedema
Proteinuria

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7
Q

Commonest cause of nephrotic syndrome (children vs adults)

A

Children - minimal change (nothing seen on light microscopy but on electron microscopy podocyte effacement seen)

Adults - Membranous (or FSGS or diabetes)

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8
Q

Define nephritic syndrome

A

Haematuria
Hypertension
Uraemia

RBC casts form (ie ‘casts’ of the tubule made from clotted blood) giving urine smoky colour

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9
Q

Causes of nephritic syndrome

A

(two classic Dxes)
Post - strep glomerulonephritis (weeks post-URTI)
Rapidly progressive glomerulonephritis (crescentic)
Goodpastures (anti-GBM)
Vaculitic (Wegner’s p/c ANCA)

IgA nephropathy (1/2 days post-URTI)
SLE
Hep B/C
Vasculitis (Henoch-Schonlein purpura)

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10
Q

Treatment of hyperkalaemia

A
Calcium Gluconate 10ml 10%
Glucose and Insulin
Salbutamol neb
Calcium Resonium
Possible dialysis?
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11
Q

ECG changes in hyperkalaemia

A

Peaked T waves (usually the earliest sign of hyperkalaemia)

P wave widens and flattens
PR segment lengthens
P waves eventually disappear

Prolonged QRS
sine wave appearance

Asystole
Ventricular fibrillation
PEA

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12
Q

Causes of hyperkalaemia

A
Renal (Failure and K+ sparing diuretics) 
Metabolic Acidosis
Addisons 
Drugs (ACEi, B-Blockers, NSAIDS)
Rhabdomyolysis
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13
Q

Post-surgery causes of reduced UO

A
Radio-contrast (Nephrotoxic)
Anaesthetic agents
Blood Loss (hypovolaemia)
Age
If vasculopath then atherosclerosis of kidney vessels
Nil by mouth for surgery
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14
Q

Features of a sick AKI patient

A
Tachycardia 
Hypotension
Oliguria 
Metabolic Acidosis
Hypoxamia
Peripheral shutdown
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15
Q

Possible tests in AKI

A
ECG (K+)
Inflam markers
Imaging (Ultrasound/CT)
Urine Dip (Protein, blood)
Microscopy
Immunology
U&Es and repeat
ABG
Bone Profile
FBC
Cultures
LFTs
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16
Q

‘Red flags’ in renal disease hx/examn

A
Acute on chronic or acute?
Renal tract obstruction
Hypovolaemia
Vascular occlusion - bruits?
Extra-renal involvement
17
Q

When should you stop and ACEi due to decreasing renal function?

A

NICE guidelines suggest if <30% raise in Cr then repeat test in 2 weeks

18
Q

Post-surgical op, a patient develops incontinence. What is the first thing to do?

A

Examine the abdomen for distended bladder

19
Q

What is a delayed nephrogram?

A

When contrast remains in a kidney for longer than a few minutes following a KUB study

20
Q

What are the indications for an acute haemodyalisis?

A

Hyperkalaemia (RESISTANT)
Uraemia (pericarditis)
Severe acidosis
Pulmonary oedema

21
Q

Following catheter insertion in an obstructed bladder, what piece of management should you initiate?

A

IV fluids - following obstruction, the kidneys kick start again and produce over a litre of urine meaning fluids are required for euvolaemia.

22
Q

What biochemical tests are altered by CKD?

A

Increase ALP, anaemia and normal K+

23
Q

What mechanism caused renal osteodystrophy?

A
CKD ->
Decreased phosphate extcretion->
Increase phosphate and decreased calcium ->
Increase PTH production ->
Renal osteodystrophy

Bone pain, deformation and fracture

24
Q

What is the commonest cause of macroscopic haematuria (esp prevalent in young men)?

A

IgA nephropathy - classically this occurs in responce to a (throat) infection

25
Q

What are some of the common risk factors of kidney disease?

A
HTN
Diabetes
CV disease
Structural renal disease
Multisystem disease with renal involvement 
Metabolic Syndrome
26
Q

What is nephritic syndrome?

A

Haematurea, proteinurea, HTN, oligurea
with rising urea and creatinine

(E.g. post-strep glomerulonephritis)

27
Q

What should you always consider when faced with a young patient with proteinurea?

A

Vasculitis - ask about nosebleeds, joint pain, eye pain, rashes

28
Q

In someone with poorly purfused kidneys, what dangerous side effect can metformin have?

A

Lactic acidosis - preform urgent ABG. Expect Kussmaul breathing

29
Q

What are the classic SLE symptoms and how can the kidneys become involved?

A

Young woman with joint pain and mouth ulcers.

SLE can result in nephritis resulting in proteinurea via glomerular damage.

30
Q

Treatment of SLE nephritis?

A

Threefold:

  1. decrease proteinurea with ACEi
  2. Manage HTN
  3. Slow renal disease with immunosupresion (steroids +/- cyclophosphamide)
31
Q

What should you be trying to rule out is a patient presents with AKI?

A

Common causes - hypovolaemia and distal obstruction

Even if the bladder is not palpable then check for a more proximal obstruction with a USS of the bladder and kidneys

32
Q

Increased VTE risk in nephrotic syndome?

A

Loss of clotting factors in urine (PTIII)

33
Q

Acture tubular necrosis

A

Worsening renal function with muddy brown casts

Underlying aetiology

34
Q

Features of renal cell carcinoma

A

Triad of haematuria, loin pain, abdo. mass
PUO
L. Varicocele from occlusion of l testicular vein

35
Q

Commonest post transplant infeciton

A

CMV

36
Q

Management of contrast in CKD3

A

IV 0.9% saline pre- and post-procedure

37
Q

Screening for ADPKD

A

US

38
Q

Mechanism of renal osteodystrophy

A

Secondary hyperparathyroidism

Worsening renal function results in decreased vit d conversion to active form. Dereased secretion of phosphate.

Hypocalcaemia therefore results

Increased PTH -> increased osteoclastic activity -> OD