CPC 5 Peripheral oedema Flashcards

1
Q

List differentials for the following patient:
Mr KA

 Swelling of legs
 Frusemide had no effect. 
 No PMH, on multivits, mother had DM
 Examination: HR 80. BP 140/80, JVP not seen. Small right pleural effusion 
in chest.
A

Congestive cardiac failure, liver failure, nephrotic syndrome,
chronic kidney disease stage IV.

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2
Q

List groups in which to consider underlying causes of peripheral oedema

A

Increased hydrostatic pressure

Decreased oncotic pressure

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3
Q

Causes of increased hydrostatic pressure leading to peripheral oedema

A

Increased intravascular pressure.

Increased lymphatic hydrostatic pressure

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4
Q

Intravascular causes of increased hydrostatic pressure

A

Heart failure
Volume overload
Venous obstruction

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5
Q

Types of heart failure

A

HF with reduced ejection fraction

HF with preserved ejection fraction.

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6
Q

Lymphatic causes of increased hydrostatic pressure leading to peripheral oedema

A

Obstruction of lymphatics:
Malignancy
Previous radiotherapy
Filariasis

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7
Q

Causes of decreased oncotic pressure leading to peripheral oedema

A

Excess protein loss (nephrotic syndrome)
Inadequate protein synthesis (liver failure)
Inadequate protein absorption (bowel, pancreas)
Inadequate protein intake.

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8
Q

Common causes of bilateral leg oedema

A

Increased hydrostatic pressure: volume overload, RHF, CCF.

Decreased oncotic pressure: chronic liver failure, nephrotic syndrome.

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9
Q

The ABC of glomerulonephropathies

A
A = aetiology (primary or secondary)
B = biopsy
C = clinical presentation
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10
Q

Primary glomerulonephropathies

A

Minimal change, membranous GN, FSGS and MCGN

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11
Q

Causes of membranous GN

A

Idiopathic in 2/3 cases, but can be associated, with drugs, SLE, HepB, HepC malaria and malignancy of a solid organ.
Anti-PLA2RI antibody has also been associated.

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12
Q

Causes of secondary glomerulonephritides.

A

Infection, autoimmune disease, diysgammaglobulinaemias, drugs and malignancy
Diabetes mellitus, amyloidosis, SLE and infection.

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13
Q

Purpose of biopsy in glomerulonephritis

A

 Gives diagnosis.

 Suggests how much damage, and reversibility.

 Directs treatment and prognosis.

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14
Q

Clinical presentation of minimal change GN

A

Proteinuria, normal GFR, normal BP

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15
Q

Clinical presentation of membranous GN

A

Proteinuria, mild renal impairment and mild hypertension.

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16
Q

Clinical presentation of FSGS

A

Proteinuria, mild renal impairment and mild hypertension.

17
Q

Clinical presentation of diffuse proliferative GN

A

Mild to severe proteinuria, renal impairment and

hypertension.

18
Q

First presentation of nephrotic syndrome

A

Frothy urine and lethargy.

19
Q

Nephrotic syndrome triad

A

Oedema, hypoalbuminaemia, proteinuria.

20
Q

Protein results for nephrotic syndrome

A

Either 24h urine protein of
>3.5g, or ACR of >220 (normal is 3.0 mg/mmol) or PCR of >300
(normal

21
Q

What are the results of loss of protein in nephrotic syndrome?

A

Frothy urine, clotting abnormalities, immunocompromised.

22
Q

Severity and results of hypoalbuminaemia in nephrotic syndrome

A

Less than 30 g/l, or less than 20 g/l if severe.

Leads to hypercholestraemia, hypercoagulable, reduced oncotic pressure leading to oedema.

23
Q

Common causes of presentation of nephrotic syndrome

A

Minimal change GN, FSGS and membranous GN (most common).

24
Q

Complications of nephrotic syndrome

A

o Thromboembolism
o Infection
o Hypercholestraemia
o Hypovolaemia.

25
Nephritic syndrome triad
Haematuria, renal impairment and hypertension.
26
Investigations into glomerulonephropathies
CRP/ESR Autoimmune serology Serum immunoglobulins Hepatitis serology
27
General treatment for nephrotic syndromes
```  Diuretics  Fluid restrict  ACEI/ARB  Aspirin  Warfarinise if albumin ```
28
Treatments for membranous GN
Chlorambucil and steroids (ponticelli regimen)  Cyclophosphamide and steroids  Tacrolimus.  Rituximab (aCD20) and Belimumab (aBAFF).
29
In heart failure, what biomarker is raised?
BNP and NTproBNP are secreted in response to ventricular stretch. Stimulate sodium and water elimination by the kidney and are elevated in heart failure. Negative BNP is a rule out for heart failure in non-treated patients.
30
Causes of HF-REF
 Myocardial infarction  Dilated cardiac myopathy (genetic, viral, autoimmune, alcohol, drugs, peripartum)  Acute myocarditis  Valvular disease  Arrhythmias
31
Causes of HF-PEF
 Left ventricular hypertrophy (secondary to hypertension)  Genetic  Infiltrative disorders inc amyloidosis and sarcoidosis.  Valvular heart disease.
32
Causes of high output heart failure
Anaemia, pregnancy, hyperthyroidis, Paget's disease, AV malformation.