Congestion and Oedema Flashcards

1
Q

What is the key thing to remember in congestion and oedema?

A

Water flows downhill, down a pressure gradient.

Things must do down a pressure gradient otherwise it won’t flow.

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2
Q

What is the critical relationship (ohm’s law)?

A
Q = deltaP/R
Q = BF, P = pressure, R = resistance.
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3
Q

What is congestion?

A

Relative excess of blood in the vessels of tissue or organ.

Passive process, secondary phenomenon (not like active inflammation where it is active hyperaemia).

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4
Q

Is congestion acute or chronic?

A

Can be either.

Can become acutely congested - e.g. when grabbed by the throat, or chronic - goes on for long time.

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5
Q

What would a congested vein in the leg look like?

A

Red, almost purple coloured, full of blood, colour difference very noticeable and swollen.

(in this case due to DVT)

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6
Q

Give the clinical categories of congestion and give examples that fall under these categories.

A

Local acute congestion, e.g. CVT
Local chronic congestion, e.g. hepatic cirrhosis
Generalise acute congestion, e.g. congestive cardiac failure.

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7
Q

Describe how DVT leads to congestion –> ischaemia and infarction.

A

Vein blocked causing local acute congestion. Blood backs up in veins, venues, capillaries. Decreased outflow of blood –> local acute congestion –> decreased pressure gradient –> decreased flow across system (Ohm’s law). So no oxygen leading to ischaemia and infarction.

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8
Q

What is hepatic cirrhosis?

A

Regenerative nodules of hepatocytes with intervening fibrosis. Results from liver damage, e.g. HBV, alcohol.

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9
Q

What happens to the normal architecture of the liver in hepatic cirrhosis? And what is the effect of this?

A

Loss of normal architecture = altered hepatic BF.
Portal BF blocked - congestion in portal vein and branches, increased portal venous pressure. Collateral circulation - several sites anastomose with systemic circulation.
Local chronic congestion.

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10
Q

What is the major risk with hepatic cirrhosis?

A

Haemorrhage risk.

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11
Q

Describe the path of hepatic blood flow?

A

Blood flows from intestines to liver then to vena cava as liver wants to get proteins and detoxify things etc…

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12
Q

What does hepatic cirrhosis look like histologically?

A

Hepatocytes in lumps, bro bands of tissue b/w. Loss of normal vascular pattern that upsets hepatic BF.

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13
Q

What are oesophageal varices?

A

Result of portal hypertension, congestion causes back up of blood so enlarged thickened vessels. If puncture this absolute firing of blood out.

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14
Q

What are caput medusae?

A

Distended and engorged superficial epigastric veins Symptom of portal hypertension (result of back up of blood from blockage in liver).

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15
Q

What can cause congestive heart failure?

AKA biventricular failure

A

When the heart is unable to clear blood (right and left ventricles) - can be due to ineffective pump, e.g. ischaemia, valve disease.

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16
Q

What is the pathophysiology of congestive cardiac failure?

A

Decreased CO, decreased renal glomerular filtrate rate –> activation of renin-angiotensin-aldosterone system –> increase in sodium and therefore water retention. So increases amount of fluid in the body. Leads to fluid overload in the veins.

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17
Q

How do you treat this overload of fluid?

A

Diuretics.

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18
Q

How is water pulled back into the kidney tubules?

A

Increased ionic retention and sodium pulled back in and water pulled back in with it.

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19
Q

What are the effects of congestive cardiac failure?

A

Heart cannot clear blood from ventricles.
Back pressure, blood dammed back in veins.
Liver - central venous congestion - right heart failure dams back into the venous system. Acute and chronic changes in lung - pulmonary oedema.

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20
Q

What signs and symptoms are you looking for in congestive cardiac failure?

A

Liver - central venous congestion: increased JVP, hepatomegaly, peripheral oedema.

Pulmonary oedema: crepitations in lungs, tachycardia (working hard to clear lot of fluid in chest).

21
Q

Describe the appearance of the liver in hepatic central venous congestion.

A

Nutmeg liver - red/brown and pale spotty appearance macroscopically.

Red = haemorrhaging, pale = poor function.

22
Q

How are the pericentral hepatocytes (red) affected in hepatic central venous congestion?

A

Stasis of poorly oxygenated blood.

23
Q

How are the periportal hepatocytes (pale) affected in hepatic central venous congestion?

A

Relatively better oxygenated due to proximity of hepatic arterioles.

24
Q

Describe the normal microcirculation.

A

Constant movement of fluid through capillary beds, process of dynamic equilibrium.
Filtration from capillary beds to interstitial.

25
Q

What forces are involved in normal circulation?

A

Driven by hydrostatic pressure from heart, balanced by osmotic pressures and endothelial permeability.
Involves lymphatics.

26
Q

What are the three components that affect net flux and filtration?

A

Hydrostatic pressure
Oncotic pressure
Permeability characteristics and area of endothelium

27
Q

What does disturbance in the normal components of microcirculation cause?

A

Oedema.

28
Q

What is Starling’s Hypothesis?

A

Net filtration (Jv)= [(force favouring filtration/flow of fluid out of vessel) - endothelial permeability to proteins x (forces opposing filtration/keeping fluid in vessel)] x endothelial permeability to H2O x area of capillary bed

29
Q

Define oedema.

A

Accumulation of abnormal amounts of fluid in the extravascular space (intracellular tissue spaces (ECP) or body cavity.

30
Q

How do peripheral oedema and effusions differ?

A

Fluid collections in body cavity = effusions.

Peripheral oedema - increased intersistal fluid in tissues.

31
Q

Give examples of effusions.

A

Pleural, pericardial, joint effusions.

Abdominal cavity = ascites.

32
Q

Describe oedema as a transudate.

A

Alterations in the haemodynamic forces which act across the capillary wall. Cardiac failure, fluid overload.
Not much protein/albumin (few cells)
Lots of water and electrolytes.
Low specific gravity.

33
Q

Describe oedema as an exudate.

A
Part of inflammatory process due to increased vascular permeability. 
Tumour, inflammation, allergy. 
Higher protein/albumin content.
Water and electrolytes. 
High specific gravity.
34
Q

What happens in pulmonary oedema?

A

Too much fluid going to the lungs, leaks out into alveoli and decreases gas exchange.

35
Q

What is the pathophysiology of pulmonary oedema?

A

Hydrostatic pressure - transudate
LVF
- increased L atrial pressure –> passive retrograde flow to pulmonary veins, capillaries and arteries.
- increased pulmonary vascular pressure
- increased pulmonary blood volume
- increased pressure –> increase filtration and pulmonary oedema

36
Q

What are the effects of pulmonary oedema in the lungs?

A

Perivascular and interstitial transudate
Progressive oedematous widening of alveolar septa
Accumulation of oedema fluid in alveolar spaces.

37
Q

Describe the pathophysiology of peripheral oedema.

A

R heart failure - cannot empty RV in systole.
Blood retained in systemic veins –> increased P in capillaries, increased filtration –> oedema.
Also secondary portal venous congestion via liver.

38
Q

What happens in congestive cardiac failure to lead to pulmonary and peripheral oedema?

A

R and L ventricles fail at same time.

All about hydrostatic pressure.

39
Q

Describe the pathophysiology of lymphatic blockage.

A

Lymphatic obstruction – hydrostatic pressure upset.

Lymphatic drainage is required for normal flow. If blocked –> lymphedema.

40
Q

When is lymphedema most common?

A

Breast cancer may req radiotherapy to axilla, which can cause fibrosis and scarring of lymph vessels, leading to blockage, decreased flow and oedema of the upper limb.

41
Q

What happens during abnormal renal function?

A

Salt and H2O retention.

42
Q

What can do you get secondary to heart failure?

A

Reduced renal BF.

43
Q

What is the reason for primary oedema in abnormal renal function?

A

Acute tubular damage, e.g. hypotension.

44
Q

What is the pathophysiology of oedema in abnormal renal function?

A

Decreased renal function, leading to increased salt and water retention, increased intravascular fluid volume, secondary increased capillary pressure –> oedema.

45
Q

Describe the pathophysiology of low protein oedema.

A

Oncotic pressure - transudate.

Hypoabluminaemia –> decreased capillary oncotic pressure –> increased filtration.

46
Q

Give examples of conditions causing low protein oedema.

A

Nephrotic syndrome –> leaky renal glomerular basement membrane, lose protein, generalise oedema.

Hepatic cirrhosis –> diffuse nodules and fibrosis in liver, liver unable to synthesise enough protein

Malnutrition –> insufficient protein intake.

47
Q

What are examples of permeability oedema?

A

Acute inflammation e.g. penumonia and burns.

48
Q

What occurs in permeability oedema?

A

Damage to endothelial lining –> increased no of pores in membrane so proteins and larger molecules as well as water leaks out.