Pathophysiology of congestion + oedema Flashcards
What is congestion?
- relative excess of blood in vessels of tissue/organ
- this is a passive process and can be acute or chronic
Examples of congestion
Local acute congestion
-deep vein thrombosis
Local chronic congestion
-hepatic cirrhosis
Generalised acute congestion
-congestive cardiac failure
How does deep vein thrombosis lead to congestion?
- In DVT, there is cclusion of the vein which causes localised acute congestion.
- Blood will back up from veins, venules + capillaries
- This will decrease outflow of blood and decrease the pressure gradient.
- It will also decrease venous return. In extreme cases, No O2 > ischaemia +infarction
What is hepatic cirrhosis?
- When the liver does not function properly due to liver damage (HBV, alcohol)
- regenerating liver forms nodules of hepatocytes with intervening fibrosis
- there is a loss of normal structure due to altered hepatic BF
- Portal BF can be blocked and congestion in the portal vein and its branches will occur. This eill increase portal venous pressure. An alternative circulation ( collateral circulation) is used which anastomoses with systemic circulation.
- If local chronic congestion, haemorrhage risk
What is congestive cardiac failure?
- When the heart is unable to clear blood in right and left ventricles ( ineffective pump,)
- CO will decrease which decrease GFR, renin-angiotensin-aldesterone system will be activated and increases Na+ & H2O retention > increasing PV
Examples that may cause an ineffective heart pump
- Ischaemic disease
- valve disease
Treatment of overload of fluid in system
diuretics
State the effects of congestive cardiac failure
- heart cannot clear blood from ventricles
- back flow of blood into veins
Pulmonary oedema
- left heart failure; blood dams back into lungs
- crepitations in lungs, tachycardia
Liver - central venous congestion
- right heart failure
- blood dams back to systemiccirculation
- raised JVP, hepatomegaly, peripheral oedema
The effect of hepatic central venous congestion on liver
Pericentral hepatocytes (red) -stasis of poorly ocygenated blood
Periportal hepatocytes (pale) - better due to oxygenated blood in close proximity of hepatic arterioles
What is an oedema?
-accumulation of fluid in the extravascular space ( body cavities, intracellular tissue compartment)
What is a peripheral oedema?
-increased ISF in tissues
What is a effusion?
- fluid collection in body cavities
- pleural, pericardial, joint effusions, ascites ( abdnominal cavity)
What is a transudate oedema?
- A filtrate of blood and can be caused due to increased pressure in veins/capillarie(changes in the haemodynamic forces)
- can be due to cardiac failure, or fluid overload
What is found in a transudate oedema?
- no protein(albumin) and has fewer cells
- Rich in water and electrolytes
- Low specific gravity
What is an exudate oedema?
-fluid rich in protein/cells
part of inflammatory process due to increase vascular permeability
-caused by tumour, inflammation and allergy
-higher protein/albumin content ( cells)
-Water an electrolytes
-high specific gravity
Describe the pathophysiology of a pulmonary oedema
-Hydrostatic pressure causes a transudate
Left ventricular failure
- pressure in left atrium to increase which causes backflow of bloos to pulmonary veins, capillaries and arteries.
-this caused raised pulmonary vascular pressure and increases pulmonary BV
-Increased capillary hydrostatic pressure increases filtration > Pul.oedema
In lungs
- perivascular and intersitial transudate
- progresssive oedematous widening of alveolar septa + accumulation of oedema fluid in alveolar spaces
Describe the pathophysioogy of a peripheral oedema
Right heart failure
- heart cannot enoty RV during systole so blood retained in systmic veins will increase pressure in capillaries + increase filtration.
- This leads to a peripheral oedema and secondary portal venous congestion via liver.
Congestive cardiac failure causes:
- R+L ventricles failure
- pul oedema/peripheral at same time
State the pathophysiology of lymphatic blockage
Lymphatic pobstruction will cause hydrostatic pressure upset
- if this is blocked, lymphoedema
- e.g. breast cancer may require radiotherapy to axilla > fibrosis which leads to a decrease in outflow > oedema of upper limb
Describe the pathophysiology of oedema in abnormal renal function
- results in salt and H2O retention
- secondary in heart failure > reduced renal BF
- primary > acute tubular damage ( eg hypotension)
- both decreases renal function
-This increases salt and H20, Intravascular fluid volume, secondary capillary hydrostatic pressure > oedema
Describe the pathophysiology of low protein oedema
Oncotic pressure - transudate
- capillary oncotic pressure requires normal protein levels
- Hypoalbuminaemia will lead to decreased capillary oncotic pressure increased fitratin
Examples of hypoalbunaemiea
Nephrotic syndrome
-leaky renal glomerular basement membrane > lose protein > oedema
Hepatic cirrhosis
-diffuse nodules and fibrosis in liver > liver unable to synthesise sufficient protein
Malnutrition
- insufficient intake of protein
Describe the pathophysiology of permeability oedema
Endothelial permeability
- damage to endothelial lining leads to an increase in ‘pores’ of membrane.
- This leads to osmotic reflection coefficient of endothelium to decrease towards 0
- proteins and larger molecules can now leak out
- caused by acute inflammation ( pneumonia, burns etc)
