Congestion and Oedema Flashcards
Define what congestion is?
Relative excess of blood in vessels of tissue or organ
Can be acute or chronic
Not active hyperaemia
Is congestion an active or passive process?
Passive
What are some clinical pathology examples of congestion?
Local acute congestion
-Deep vein thrombosis
Local chronic congestion
-Hepatic cirrhosis
Generalised acute congestion
-Congestive cardiac failure
Define and describe the pathophysiology behind deep vein thrombosis?
Veins blocked causing localised acute congestion
Blood backs up in the veins, venules and capillaries.
Reduced outflow of blood so causes congestion.
This leads to decrease in pressure gradient and flow across system
No O2 = ischaemia and infarction
Define and describe the pathophysiology behind hepatic cirrhosis?
Results from serious liver damage eg: HBV, alcohol
Regenerating liver forms nodules of hepatocytes with intervening fibrosis
This causes;
- Loss of normal architecture:
- altered hepatic blood flow - Portal blood flow blocked
- congestion in portal vein and branches
- increased portal venous pressure
- collateral circulation: several sites anastomose with systemic circulation - Local chronic congestion
- haemorrhage risk
CONSEQUENCE = portant systemic shunts
Define and describe the pathology behind congestive cardiac failure?
Heart unable to clear blood, right and left ventricles
due to ineffective pump ischaemia or valve disease
Therefore =
- Decreased cardiac output
- Decreased renal glomerular filtreation rate
- activation of RAAS
- Increase Na and H2O retention - Increase amount of fluid in body
An increase in fluid (overload) in veins
Treatment is diuretics
What are the effects of congestive cardiac failure?
- Heart cannot clear blood from ventricles
- Back pressure, blood dammed back in veins
- Lungs (pulm oedema):
- LHF: blood dams back into lungs
- Clinically, crepitations in lungs, tachycardia - Liver (central venous congestion)
- RHF - blood dams back to systemic circulation
- Increase JVP, hepatomegaly, peripheral oedema
What is hepatic central venous congestion?
Nutmeg liver=brown/red and pale spotty appearance macroscopically
- Pericentral hepatocytes (red) = stasis of poorly oxygenated blood
- Periportal hepatocytes (pale) = relatively better oxygenated due to proximity of hepatic arterioles
What is the micro circulation like normally?
- Constant movement of fluid through capillary beds; process of dynamic equilibrium
- Its driven by hydrostatic pressure from heart
- Balanced by osmotic pressures and endothelial permeability
- Filtration from capillary beds to interstitium
In summary:
3 factors effect net flux and filtration: Hydrostatic, oncotic pressure and permeability/area of endothelium
Define oedema?
Accumulation of abnormal amounts of fluid in the extravascular compartment
- intercellular tissue compartment (extracellular fluid)
- body cavities
Define what peripheral oedema is?
Increased interstitial fluid in tissues
What are effusions?
Fluid collections in body cavities
- pleural,pericardial,join effusions
- Abdominal cavity: ascites
What is the pathophysiology behind oedema transudate?
Alterations in the haemodynamic forces which act across the capillary wall Cardiac failure, fluid overload Not much protein/albumin Lots of H20 and electrolytes Low specific gravity
What is the pathophysiology behind oedema exudate?
Part of inflammatory process due to increased vascular permeability
Tumour, Inflammation, allergy
Higher protein/albumin content
H2O and electrolytes
What is the pathophysiology of pulmonary oedema
Hydrostatic pressure - transudate
- Left ventricular failure:
- Increase in left atrial pressure -> passive retrograde flow to pulm veins, capillaries and arteries
- Increased pulm vascular pressure
- Increased pulm blood volume
- Increase Pc causes Increased filtration and pulm oedema
In lungs
- Perivascular and interstitial transudate
- Progressive oedematous widening of alveolar septa
- accumulation of oedema fluid in alveolar spaces
What is the pathophysiology behind peripheral oedema?
RHF = cannot empty RV in systole
Therefore, blood retained in systemic veins -> Increase P in capillaries -> Increased filtration -> Peripheral oedema
*Also secondary portal venous congestion via liver
-JVP increased
-Congestive cardiac failure causes =
Both R and LV to fail
Pulm oedema and peripheral oedma at the same time
All about hydrostatic pressure
What is the pathophysiology behind lymphathic blockage and give an example?
Hydrostatic pressure upset due to obstruction in lympathics
-Drainage needed for norm flow
-If blocked this causes lymphoedema
eg; breast cancer may require radiotherapy to axilla -> fibrosis -> decreased outflow -> oedema of upper limb
What is the pathophysiology behind oedema in abnormal renal function?
Abnormal function in renal casues retention of salt and H2O
Secondary in heart failure = reduced renal blood flow
Primary: Acute tubular damage due to hypotension
Decreased renal function is the result of both:
- Increased salt and H20
- Increased intravascular fluid volume
- Secondary Increased Pc
- Oedema
What is the pathophysiology of low protein oedema?
Oncotic pressure - transudate
Oncotic pressure (c) needs normal protein level so if hypoalbuminaemia -> Decrease oncotic pressure (capillary) and increase filtration
For example:
- Nephrotic syndrome -> leaky renal glomular basement membrane; lose protein; generalised oedema
- Hepatic cirrhosis -> diffuse nodules and fibrosis in liver; liver cant synthesis enough protein
- Malnutrition -> insufficient intake of protein (increase Jugular vein presssure)
In the terms of hydrostatic and oncotic pressure, which pressure is bigger on the arterial side?
Capillary hydrostatic pressure > Capillary oncotic pressure
Therefore, mostly filtration occurs
In the terms of hydrostatic and oncotic pressure, which pressure is bigger on the venous side?
Capillary oncotic pressure > capillary hydrostatic pressure
Therefore, mostly reabsorption occurs
What is the pathophysiology behind permeability of oedema?
Endothelial permeability - exudate
- Damage to endothelial lining leads to increase in pores in membrance -> decrease of osmotic reflection coefficient of endothelium towards zero
- Proteins and larger molecules can leak out (not just H2O)
eg: acute inflammmation such as pneumonia
eg: burns
Increase Jv
