Pathophysiology of congestion and oedema Flashcards

(31 cards)

1
Q

What is congestion?

A

relative excess of blood in vessels of tissue or organ

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2
Q

Give characteristics of congestion?

A

passive process
acute or chronic

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3
Q

Describe deep vein thrombosis of the leg?

A

because vein is blocked
blood backs up in veins
blocks the venules and capillaries downstream
outflow of blood through proximal vessel is blocked and cause local acute congestion
pressure gradient across limb is reduced
resistance remains same
flow goes down as flow is proportionate to difference in pressure (blood flow= difference in pressure/ resistance)
no blood flow means no oxygen and therefore ischemia and infarction development

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4
Q

What does hepatic cirrhosis result from?

A

serious liver damage e.g. HBV, alcohol

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5
Q

What happens in hepatic cirrhosis?

A

liver gets damaged and get regeneration of the liver and this forms nodules of liver cells, hepatocytes and intervening fibrosis.

Loss of normal architecture- alteration in hepatic blood flow

Blockage of portal blood flow
-congestion in portal vein (Vein from digestive organs to liver) and branches
-increased portal venous pressure
- then get collateral circulation-several sites of portal vein anastomose with systemic circulation

Result of this is that there is local chronic congestion in the gut and veins- find very small vessels with small thin walls dilated and increasing pressure - haemorrhagic risk

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6
Q

What is congestive cardiac failure?

A

heart is dysfunctional and cant clear blood from right and left ventricles. Ineffective pump

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7
Q

Where do you see congestive heart failure?

A

ischaemia and valve disease

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8
Q

What is the pathophysiology of congestive cardiac failure?

A

cardiac output is reduced
and reduced flow through glomeruli -> activates RAAS and effect of that is it increases sodium and water retention in the body
too much fluid in vessels
and get too much blood flowing to heart- which can’t be pumped out

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9
Q

What are the effects of cardiac failure?

A

heart cannot clear blood from ventricles
blood dammed back in veins

lungs- pulmonary oedema
-left heart failure- blood dams back into lungs
-clinically crepitations in lungs, tachycardia

right heart failure- blood dams back to systemic circulation
- liver is first thing affected
-raised JVP
- feel hepatomegaly
-see peripheral oedema

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10
Q

What does congested liver look like?

A

red brown and pale spots

red areas- further from oxygen rich blood

pale areas- closer to oxygenated blood

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11
Q

Describe normal microcirculation?

A

capillaries- interstitium- capillaries and lymphatics

constant movement of fluid through capillary bed; process of dynamic equilibrium

driven by hydrostatic pressure from heart

balanced by osmotic pressures and endothelial permeability

filtration from capillary beds to interstitium

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12
Q

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

A

hydrostatic pressure
oncotic pressure
permeability characteristics and area of endothelium

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13
Q

What is oedema?

A

accumulation of abnormal amounts of fluid in the extravascular compartment
- intercellular tissue compartment
-body cavities

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14
Q

When is it called peripheral oedema?

A

tissues

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15
Q

When is it called effusions?

A

body cavities

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16
Q

What is ascites?

A

Peritoneal fluid effusion

17
Q

Give characteristics of oedema as a transudate?

A

-transudate
-result of alterations in the haemodynamic forces which across the capillary wall
-not much protein/ albumin
-lots of water and electrolytes

17
Q

Give characteristics of oedema as an exudate?

A

part of inflammatory process and due to increased vascular permeability

tumour, inflammation, allergy

higher protein/ albumin content

water and electrolytes

high specific gravity

18
Q

Describe pathophysiology of pulmonary oedema?

A

hydrostatic pressure-transudate

in left ventricular failure: ventricle can’t get rid and and there’s damming back into left atrium

increased left atrium pressure and means will pass back through pulmonary veins and to pulmonary artery

increased pulmonary vascular pressure

increased pulmonary blood volume

increase in pressure in pulmonary capillaries - then pushed into p interstitium

18
Q

Describe what happens to pulmonary oedema in the lungs?

A

perivascular and interstitial transudate
progressively alveolar septa widen and spill over into alevolar spaces

19
Q

Pathophysiology of peripheral oedema?

A

failure of RV and so have blood backing up into RA

backs up into systemic veins - increased pressure in capillaries-increased filtration and peripheral oedema
(also see secondary portal venous congestion via liver)

20
Q

Describe congestive cardiac failure?

A

right and left ventricles both fail
pulmonary and peripheral oedema at same time

21
Q

Describe pathophysiology of lymphatic blockage?

A

lymphatic obstruction-
hydrostatic pressure upset
as lymphatics are responsible for draining fluid out of the intestitium and back into venous circulation

if lymphatics blocked- lymphoedema

22
Q

Why is upper limb oedema observed in giving radiotherapy to axilla?

A

breast cancer in axilla( contains a lot of lymphatic channels).
Radiation produces fibrosis and reducing outflow

23
Describe pathophysiology of oedema in abnormal renal function?
abnormal renal function results in salt and water retention secondary in HF- reduced renal blood flow primary: acute tubular damage eg hypotension decreased renal function activates the RAAS and produces salt and water retention, increased intravascular volume- increased Pc and drives flux from vessels into periphery.
24
Describe pathophysiology of low protein oedema?
oncotic pressure- transudate capillary oncotic pressure requires normal protein levels - so if reduce amount of capillary pressure- increase filtration
25
Describe nephrotic syndrome?
leaky renal glomerular basement membrane and lose protein and get generalized oedema
26
describe hepatic cirrhosis?
diffuse nodules and fibrosis in liver and liver unable to synthesize enough protein
27
Describe how malnutrition leads to oedema?
dont have enough AA to make proteins for oncotic pressure
28
Pathophysiology of permeability oedema?
endothelial permeability- exudate damage to endothelial lining increases "pores" in membrane proteins and larger mols just leak out acute inflammation such as pneumonia, burns
29