CPC 5 Peripheral oedema Flashcards Preview

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Flashcards in CPC 5 Peripheral oedema Deck (32):
1

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.

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

2

List groups in which to consider underlying causes of peripheral oedema

Increased hydrostatic pressure
Decreased oncotic pressure

3

Causes of increased hydrostatic pressure leading to peripheral oedema

Increased intravascular pressure.
Increased lymphatic hydrostatic pressure

4

Intravascular causes of increased hydrostatic pressure

Heart failure
Volume overload
Venous obstruction

5

Types of heart failure

HF with reduced ejection fraction
HF with preserved ejection fraction.

6

Lymphatic causes of increased hydrostatic pressure leading to peripheral oedema

Obstruction of lymphatics:
Malignancy
Previous radiotherapy
Filariasis

7

Causes of decreased oncotic pressure leading to peripheral oedema

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

8

Common causes of bilateral leg oedema

Increased hydrostatic pressure: volume overload, RHF, CCF.
Decreased oncotic pressure: chronic liver failure, nephrotic syndrome.

9

The ABC of glomerulonephropathies

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

10

Primary glomerulonephropathies

Minimal change, membranous GN, FSGS and MCGN

11

Causes of membranous GN

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.

12

Causes of secondary glomerulonephritides.

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

13

Purpose of biopsy in glomerulonephritis

 Gives diagnosis.

 Suggests how much damage, and reversibility.

 Directs treatment and prognosis.

14

Clinical presentation of minimal change GN

Proteinuria, normal GFR, normal BP

15

Clinical presentation of membranous GN

Proteinuria, mild renal impairment and mild hypertension.

16

Clinical presentation of FSGS

Proteinuria, mild renal impairment and mild hypertension.

17

Clinical presentation of diffuse proliferative GN

Mild to severe proteinuria, renal impairment and
hypertension.

18

First presentation of nephrotic syndrome

Frothy urine and lethargy.

19

Nephrotic syndrome triad

Oedema, hypoalbuminaemia, proteinuria.

20

Protein results for nephrotic syndrome

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

21

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

Frothy urine, clotting abnormalities, immunocompromised.

22

Severity and results of hypoalbuminaemia in nephrotic syndrome

Less than 30 g/l, or less than 20 g/l if severe.
Leads to hypercholestraemia, hypercoagulable, reduced oncotic pressure leading to oedema.

23

Common causes of presentation of nephrotic syndrome

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

24

Complications of nephrotic syndrome

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.