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
Q

Nephritic syndrome triad

A

Haematuria, renal impairment and hypertension.

26
Q

Investigations into glomerulonephropathies

A

CRP/ESR
Autoimmune serology
Serum immunoglobulins
Hepatitis serology

27
Q

General treatment for nephrotic syndromes

A
 Diuretics
 Fluid restrict
 ACEI/ARB
 Aspirin
 Warfarinise if albumin
28
Q

Treatments for membranous GN

A

Chlorambucil and steroids (ponticelli regimen)
 Cyclophosphamide and steroids
 Tacrolimus.
 Rituximab (aCD20) and Belimumab (aBAFF).

29
Q

In heart failure, what biomarker is raised?

A

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
Q

Causes of HF-REF

A

 Myocardial infarction

 Dilated cardiac myopathy (genetic, viral, autoimmune, alcohol, drugs, peripartum)

 Acute myocarditis

 Valvular disease

 Arrhythmias

31
Q

Causes of HF-PEF

A

 Left ventricular hypertrophy (secondary to hypertension)

 Genetic

 Infiltrative disorders inc amyloidosis and sarcoidosis.

 Valvular heart disease.

32
Q

Causes of high output heart failure

A

Anaemia, pregnancy, hyperthyroidis, Paget’s disease, AV malformation.