Pathophysiology of Congestion and Oedema Flashcards

1
Q

What is congestion?

A

Relative excess of blood in vessels of a tissue or organ, a passive process

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2
Q

What is the first thing noticed in congestion?

A

Colour difference - red, almost purple in colour

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3
Q

Examples of local acute congestion

A

DVT

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4
Q

Example of local chronic congestion

A

Hepatic cirrhosis (liver fibrosis)

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5
Q

Example of generalised acute congestion

A

Congestive cardiac failure

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6
Q

When does congestive heart failure?

A

Occurs when the heart is unable to clear blood, from both the right and left ventricles due to an ineffective pump (e.g. valve disease, ischaemia)

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7
Q

Pathology of congestive heart failure

A

Decrease in CO
Decreased GFR activates RAAS system leads to increased Na and H20 retention
Increased amount of fluid in the body
Results in fluid overload in the veins - congestion.

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8
Q

What is the treatment for fluid overload in the body?

A

Diuretics

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9
Q

Effects of congestive heart failure

A

Heart cannot clear blood from ventricles
Back pressure in the system, blood dammed back into the veins
Liver gets central venous congestion, which leads to right heart failure and increased JIV, hepatomegaly and peripheral oedema
Acute and chronic changes in lungs - pulmonary oedema. Left heart failure and shows clinically by tachycardia and creps in the lungs

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10
Q

What does the liver look like in hepatic central venous congestion?

A

“Nutmeg Liver” - brown/red and pale spotty appearance
Red pericentral hepatocytes - stasis of poorly oxygenated blood
Periportal hepatocytes (pale) - relatively better oxygenated due to proximity of hepatic arterioles

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11
Q

Causes of vascular congestion

A

DVT of leg

Hepatic cirrhosis

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12
Q

What is a consequence of vascular congestion?

A

Systemic portal shunts

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13
Q

Pathology of DVT

A

Blocked vein
Blood backs up the veins, venules and capillaries
This decreases the outflow of blood
Local, acute congestion
Decreased pressure gradient across the capillary beds
Decreased flow across the system
No oxygen leads to ischaemia and infarction (venous infarction common in gut and rare in DVT)

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14
Q

Pathology of Hepatic cirrhosis as a chronic congestive process

A

Regenerative nodules of hepatocytes with intervening fibrosis
Results from liver damage
Loss of normal architecture leads to altered hepatic blood flow
The portal blood flow then gets blocked due to congestion in the portal vein and branches causing increased portal venous pressure. Also in the collateral circulation several sites anastomose with systemic circulation. This therefore disrupts function of the gut
Local chronic congestion and therefore haemorrhage risk

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15
Q

Examples of systemic portal shunts

A

Oesophageal varices

Caput medusae

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16
Q

What is a very serious risk with systemic portal shunts?

A

Haemorrhage

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17
Q

Where are caput medusae found?

A

Around the umbilicus

18
Q

Transudate vs exudate oedema

A

Transudate - alterations in the haemodynamic forces which act across the capillary wall due to high forces in the capillary
Exudate - Part of the inflammatory process due to an increased vascular permeability - leaks around the cells of the capillaries due to inflammation

19
Q

Features of transudate oedema

A

Cardiac failure, fluid overload
Not much protein/albumin
Lots of H20 and electrolytes
Low specific gravity

20
Q

Features of exudate oedema

A

Tumour, allergen, inflammatory
Higher protein content/albumin content
H20 and electrolytes
High specific gravity

21
Q

Describe the normal microcirculation

A

Constant movement of fluid through capillary beds; process of dynamic equilibrium
Driven by hydrostatic pressure from heart
Balanced osmotic pressures and endothelial permeability
Filtration from capillary beds to interstitium
Venous end tends to pull back into the vessel

22
Q

What are the 3 components affecting net flux and filtration

A
  1. Hydrostatic pressure
  2. Oncotic pressure
  3. Permeability characteristics and area of endothelium
23
Q

Disturbances of normal components leads to what?

A

Oedema

24
Q

Definition of oedema

A

Accumulation of abnormal amounts of fluid in extravascular compartment

25
Q

Examples of extravascular compartment

A

Intercellular tissue compartment (extracellular fluid)

Body cavities

26
Q

What is peripheral oedema?

A

Increased interstitial fluid in tissues

27
Q

Definition of effusions

A

Fluid collections in body cavities

28
Q

Examples of body cavities where you can get effusions

A

Pleural
Pericardial
Joints
Ascites

29
Q

Fluid in the ECF is called what?

A

Oedema

30
Q

Fluid in body cavities Is called what?

A

Effusion

31
Q

What kind of oedema is a pulmonary oedema?

A

Transudate

32
Q

Pathology of pulmonary oedema

A

Hydrostatic pressure - transudate
Left ventricular failure
- increase in left atrial pressure leads to passive retrograde flow to pulmonary vein, capillaries and arteries
- increase in pulmonary vascular pressure
- Increase pulmonary blood flow
- increase Pc leads to increased filtration and pulmonary oedema
- reduced pressure gradient across lungs as left ventricle is not being cleared
Lungs
- Perivascular and interstitial transudate
- progressive oedematous widening of alveolar septa - capillary lumen flux because of greater pressure gradient means fluid flowing into the surrounding tissue
- accumulation of oedema fluid in alveolar spaces as the fluid spills out and floods the alveoli

33
Q

Pathology of peripheral oedema

A

Right heart failure
- cannot empty right ventricle in systole
Blood retained in systemic veins leads to an increased pressure in capillaries, leading to increased filtration and flux into the interstitium and therefore peripheral oedema
Also secondary portal venous congestion via liver
Congestive cardiac failure
- right and left ventricles fail
- pulmonary oedema and peripheral oedema at same time
- all about hydrostatic pressure

34
Q

Pathology of lymphatic blockage

A

Lymphatic blockage can lead to hydrostatic pressure upset

- lymphatic drainage required for normal flow - blockage leads to lymphoedema

35
Q

Pathology of oedema in abnormal renal function

A

Abnormal renal function leads to salt and H20 retention
Secondary in HF; reduced renal blood flow
Primary; acute tubular damage e.g. hypotension
Decreased renal function is the result of both
- increased salt and H20 retention
- increased intravascular fluid volume
- secondary to an increase in Pc
leading to oedema

36
Q

Pathology of low protein oedema

A

Oncotic pressure - transudate
Normal oncotic pressure requires protein levels and other things to make it work - loss of protein results in fluid flux across the capillaries
Hypoalbuminuria results in increased filtration e.g. in
- nephrotic syndrome
- hepatic cirrhosis
- malnutrition

37
Q

How can hepatic cirrhosis lead to hypoalbuminuria?

A

Liver unable to synthesise enough protein

38
Q

Pathology of permeability oedema

A

Endothelial permeability - exudate
Damage to the endothelial lining increased “pores” in membranes and the osmotic reflection coefficient of the endothelium decreases towards 0
Proteins and larger molecules can leak out
e.g.
- acute inflammation such as pneumonia
- burns

39
Q

The upset of what forces can lead to oedema?

A

Starling forces

40
Q

What is pulsus paradoxus and what condition is it seen in?

A

Cardiac tamponade

Abnormally large drop in BP during inspiration

41
Q

What is cor pulmonale?

A

Hypertrophy of the right ventricle and right heart failure that are caused by pulmonary arterial hypertension