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1ST YEAR SYSTEMS: Cardiovascular > Congestion and oedema > Flashcards

Congestion and oedema Flashcards

1
Q

define congestion

A

Relative excess of blood in vessels of tissue or organ

- secondary phenomenon- usually occurs as a result of primary pathology

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2
Q

how is congestion dissimilar to acute inflammation?

A

Congestion is passive whereas acute inflammation is active hyperaemia.

Congestion may be associated with active hyperaemia - it can be acute or chronic

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3
Q

example of clinical pathology example of local acute congestion

A

deep vein thrombosis

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4
Q

example of clinical pathology example of local chronic congestion

A

Hepatic cirrhosis - scarring/fibrosis of liver - scar tissue prevents normal function. Liver is unable to clear toxins from the blood

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5
Q

example of clinical pathology example of generalised acute congestion

A

congestive heart failure

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6
Q

effects of deep vein thrombosis of the leg on blood flow

A

blood backs up in veins, venules and capillaries
there is a decreased outflow of blood
decrease in pressure gradient because the pressure rises

no O2 leads to ischaemia and venous infarction (uncommon form of stroke)

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7
Q

effects of hepatic cirrhosis on blood flow

A

cells in the liver become damaged as well as the surrounding supportive structures. This loss of normal architecture means altered hepatic blood flow as cells promote flow of blood around them - different route

portal blood flow becomes blocked - congestion in portal vein and branches causes an increase in portal venous pressure

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8
Q

what risk is there of local chronic congestion in hepatic cirrhosis?

A

haemorrhage risk

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9
Q

What do you see as a consequence of portal vein hypertension?

A

portal-systemic shunts

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10
Q

what is a portosystemic shunt

A

because the pressure in the portal system is so high, blood goes backwards through veins to get into the systemic circulation. It means blood bypasses the liver.

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11
Q

2 clinical signs of portal-systemic shunts

A

caput medusae

oesophageal varices

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12
Q

caput medusae

A

swollen superficial epigastric veins seen on the abdomen

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13
Q

oesophageal varices

A

dilated submucosal veins in lower part of oesophagus

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14
Q

What happens with congestive heart failure

A

the heart is unable to clear blood from the right and left ventricles. It becomes an ineffective pump and leads to ischaemia or valve disease etc

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15
Q

Pathophysiology of congestive heart failure

A

decreased cardiac output
decreased glomerular filtration rate - activate renin-angiotensin aldosterone system to increase MAP
increased fluid due to H20 retention so more fluid in veins.

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16
Q

effects of congestive heart failure in regards to the lungs

A

left heart failure causes blood to dam back into the lungs causing pulmonary oedema

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17
Q

what would you find on examination of person with congestive cardiac failure?

A

rattling/crackling sound in lungs

tachycardia

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18
Q

effects of congestive heart failure in regards to the liver

A

right heart failure causes blood to dam back into systemic circulation which causes central venous congestion. An increased JVP, hepatomegaly (abnormal enlargement of the liver) and peripheral oedema can occur

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19
Q

macroscopic sign of hepatic central venous congestion

A

nutmeg liver - red/brown and pale spotty appearance

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20
Q

Define oedema

A

Accumulation of abnormal amounts of fluid in the extravascular compartment ie intercellular tissue compartment (ECF) or body cavities

21
Q

what is peripheral oedema

A

increased interstitial fluid in tissues

22
Q

define an effusion and where you can get these

A

fluid collections in body cavities

Pleural, pericardial, joint effusions, or Abdominal cavity

23
Q

what is the normal fluid movement through capillaries driven and balanced by

A

driven by hydrostatic pressure from the heart and balanced by oncotic pressures and endothelial permeability

24
Q

what does disturbances in the normal components of fluid movement lead to?

A

oedema

25
Q

What is starling’s hypothesis

A

fluid movement due to filtration across the wall of a capillary is dependent on the balance between the hydrostatic pressure gradient and the oncotic pressure gradient across the capillary

26
Q

what is a transudate

A

an ultrafiltrate of plasma that contains few, if any, cells and doesn’t contain large plasma proteins - has H20 and electrolytes

27
Q

What is an exudate

A

mass of fluid and cells that have seeped out of blood vessels or an organ

28
Q

when is it most common for an exudate to arise

A

occurs especially in inflammation due to increased vascular permeability

29
Q

out of transudate and exudate which has a low and which has a high specific gravity

A

transudate - low

exudate - high (means that it is denser than water)

30
Q

how/ why does a transudate come about?

A

due to alterations in the haemodynamic forces which act across the capillary wall

31
Q

what can cause an overload of fluid due to high vascular hydrostatic pressure or low oncotic pressure

A

cardiac failure

32
Q

what is pitting oedema

A

often due to water retention as a result of peripheral oedema

after pressure is applied to a small area, the indentation persists after the release of the pressure

33
Q

how can left ventricular failure cause pulmonary oedema?

A

it increases L atrial pressure as result of blood not being pumped out of the heart by LV

passive backwards flow of blood to the pulmonary veins, capillaries and arteries

increase in pulmonary vascular pressure and blood volume

therefore increased capillary hydrostatic pressure meaning an increase in fluid and solute being pushed out of the vessel into the interstitial space and so more filtration and pulmonary oedema

34
Q

How does oedema arise in the lungs between alveoli

A

perivascular and interstitial transudate

caused by progressive oedematous widening of alveolar septa so oedema accumulates in the alveolar spaces

35
Q

peripheral oedema caused by right heart failure

A

cannot empty RV in systole

Blood retained in systemic veins so pressure in capillaries increases causing more filtration –> peripheral oedema

36
Q

when might you get peripheral and pulmonary oedema occuring at the same time?

A

in person with congestive cardiac failure - both the L and R ventricles fail

37
Q

why is lymphatic drainage so important

A

it is required for normal flow

38
Q

what is the oedema called cause when the lymphatic system becomes blocked

A

lymphoedema

39
Q

abnormal renal function and oedema

A

Abnormal renal function results in Salt (NaCl) and H2O retention which increases intravascular fluid volume and capillary hydrostatic pressure

40
Q

low protein oedema

A

transdute due to oncotic pressure decreasing meaning water isn’t being pulled into the circulatory system
this is all due to low protein levels in blood

41
Q

what 3 conditions could bring about low protein oedema

A

nephrotic syndrome
malnutrition
hepatic cirrhosis - liver can’t synthesise enough protein

42
Q

how does endothelial permeability come about? - exudate

A

damage to endothelial lining increases number of pores in membrane
proteins and larger molecules can leak out, not just H20

e.g acute inflammation or burns

43
Q

what is Darcy’s law?

A

Q = change in P/R

Q = blood flow
P = pressure
R= resistance
44
Q

what does it mean that congestion is a secondary phenomenon?

A

secondary to something else going on, it is not a primary pathology

45
Q

3 examples of pathology in local acute congestion, local chronic congestion and generalised acute congestion

A

local acute congestion - deep vein thrombosis
local chronic congestion - hepatic cirrhosis
generalised acute congestion - congestive cardiac failure

46
Q

what happens to form transudate and exudate?

A

increased hydrostatic pressure (pressure exerted by blood onvessel wall) pushes H20 out of the vessel

or
decrease in oncotic pressure where H20 moves from high to low pressure out of the vessel.

The reason there is more protein in an exudate is because there is often a decrease in oncotic pressure in this and it is also often due to inflammation. Inflammation causes the capillaries to be more leaky (larger pores) which allow movement of large proteins like albumin

47
Q

values for protein content in an exudate

A

> 35 g/L

48
Q

values for protein content in an transudate

A

<25 g/L

1ST YEAR SYSTEMS: Cardiovascular (39 decks)

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