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Haemodynamic disorders (disorders of circulation) Flashcards

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1
Q

What is hyperaemia?

A

Arterial vasodilation resulting in more blood in blood vessels

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2
Q

What is congestion?

A

Venous outflow obstruction resulting in more blood in blood vessels

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3
Q

Types of hyperaemia

A

Physiological
- nervous impulse (blushing)
- functional demand -> muscles, during exercise

Pathological
- acute inflammation

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4
Q

Types of congestion

A

Localised
- deep vein thrombosis (DVT)

Generalised
- congestive heart failure
- heart fails as pump -> blood flow brought in by pulmonary veins undergo block

Congested organs
- result of congestive heart failure
- enlarged
- cyanotic
- firm and heavy

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5
Q

What is an oedema?

A

An excessive extravascular accumulation of fluid in interstitial tissues/body cavities

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6
Q

What are the pri causes of oedema?

A

Changes in Starling’s forces
- increased hydrostatic pressure
- reduced oncotic (osmotic) pressure
- increased endothelial permeability -> fluid leak out of vessel into tissue space
- lymphatic obstruction -> lymphatic sys drain fluid that can’t make it back into circulation
- Na and H2O retention

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7
Q

Classification of oedema

A

Localised

Generalised

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8
Q

Causes of localised oedema

A

Impaired venous drainage
- eg: venous occlusion due to thrombosis

Increased vascular permeability and hyperaemia
- eg: inflammation

Obstruction/destruction of lymphatics
- eg: filariasis, cancer

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9
Q

Why does impaired venous drainage lead to oedema?

A

Arterial flow can get in but venous flow cannot get out -> congestion -> increased hydrostatic pressure

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10
Q

Causes of generalised oedema

A

Cardiac cause

Renal cause

Hepatic cause

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11
Q

How does cardiac oedema happen?

A

Due to heart failure
- LHF -> congestion in pulmonary veins causing increase in hydrostatic pressure in pulmonary circulation -> fluid accumulation in lungs -> pulmonary oedema
- RHF -> systemic veins get congested -> congestion in dependent parts of body like lower limbs -> hydrostatic pressure in venous sys very high -> fluid leak out -> oedema

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12
Q

What is nephrotic syndrome?

A

Protein loss in urine due to glomerular disease

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13
Q

Pathogenesis of nephrotic syndrome

A

Reduced plasma oncotic pressure -> fluid lost into extravascular compartment by Starling’s forces -> oedema fluid accumulates in peritoneal cavity and gravity-dependent lower limbs

RAA sys activated -> kidney retains Na and H2O -> worsen oedema

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14
Q

What is the diff btw exudate vs transudate?

A

Exudate
- high protein content
- plasma and fibrinogen
- many inflammatory cells

Transudate
- low protein content
- albumin but no fibrinogen
- few inflammatory cells

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15
Q

Causes of haemorrhage

A

Traumatic

Spontaneous
- abnormal vessels
- platelets
- thrombocytopenia
- qualitative platelet defect
- coagulation factor deficiency

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16
Q

What is petechiae?

A

Small red dots

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17
Q

What is purpura?

A

Large red dots

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18
Q

What is petechiae usually due to?

A

Platelet deficiency

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19
Q

What is purpura usually due to?

A

Fragile blood vessels

Coagulation factor deficiency

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20
Q

What is ecchymoses?

A

Big bruises

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21
Q

What causes bleeding into joints?

A

Coagulation defects

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22
Q

How does the body initially respond to blood loss?

A

Maintenance of BP and flow by activating sympathetic nervous sys (heart beat faster and vessels vasoconstrict) / catecholamines (produced from adrenal medulla)

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23
Q

How does body compensate for vol loss?

A

Fluid retention via aldosterone, ADH

Redistribution of blood flow to vital organs

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24
Q

How does body respond to blood loss in the long term?

A

Replacement of red cells
- dependent on fning bone marrow

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25
What are the consequences of unresolved blood loss?
Acute (severe) - shock Chronic - anemia
26
What is shock?
A state of inadequate perfusion and tissue hypoxia due to inadequate cardiac output/effective circulating blood vol
27
What are the diff types of shock?
Hypovolemic shock - due to loss of volume Cardiogenic shock - pump failure Septic shock - due to generalised vasodilation - aka distributive shock
28
What is the pathophysiology of septic shock?
Microbial antigens (i.e: lipopolysaccharide of endotoxins) bind to endotoxin receptors of macrophages -> produce cytokines -> vasodilation -> decrease cardiac contractility -> endothelial cell activation and injury -> abnormal blood coagulation (DIVC)
29
Early signs of shock
Skin -> pale and cold Kidneys -> low uring pdtn Gut -> bowel stasis Lung -> tachypnea Liver -> fatty change Brain -> reduced conscious level Heart -> tachycardia
30
What happens as shock progresses?
Multi organ fialure Cyanosis Necrosis Coma
31
Protocol for shock
Time sensitive
32
What are the vicious cycles of shock?
Heart: myocardial damage -> heart failure Gut: mucosal damage -> loss of fluid, liberation of bacteria -> more vasodilation Liver: impaired lactate catabolism -> acidosis -> impairs cardiovascular fn Kidney: acute tubular necrosis -> renal failure -> acidosis -> impairs microcirculation Lung: alveolar damage -> decreased oxygenation
33
What are the factors affecting the prognosis of shock?
Type and cause of shock Prior condition of the pt/co-morbidities Timeliness and effectiveness of treatment
34
Definition of thrombus
An intravascular blood clot formed during life
35
Definition of thrombosis
The process in which a thrombus is formed
36
What is Virchow's triad?
3 key factors that increases thrombotic tendencies Endothelial damage - damage to endothelial wall promotes clot formation Altered blood flow (stasis) - slow blood flow reduces propensity of anti-coagulants to interact w/ coagulation factors Hypercoagulability - thrombophilia -> conditions that increase tendency for clot formation
37
Pathophysiology of venous thrombosis
Stasis -> build up of activated clotting factors -> deep vein thrombosis (DVT) (blood clot in the legs)
38
Where is arterial thrombosis most often seen?
In setting of atheromatous disease
39
What are some common clinical states that can lead to thrombosis?
Atrial fibrillation Prosthetic cardiac valves Post-operative/post-partum state Prolonged bed rest/immobilisation Disseminated cancer Oral contraceptive (oestrogen)
40
Signs of local vascular occlusion
Local swelling Pain
41
What is embolization?
Thrombus travels elsewhere and cause vascular occlusion
42
What is the clinical significance of thrombosis in arteries?
Thrombus in artery -> arterial occlusion -> ischemia
43
What are some possible outcomes of a thrombus?
Resolution/lysis - body's fibrinolysis get rid of blood clot naturally Propagation - extension of thrombus to form more complete occlusion of blood vessel - possible to survive due to alternate blood flow Organisation - thrombus removed and replaced by granulation tissue and fibrosis Recanalisation - new blood vessels being formed -> restore a lot of blood flow Embolism - thrombus travel to another part of body
44
What is an embolus?
A detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin
45
Types of thrombus and some eg
Solid - detached thrombus - tissue fragments Liquid - fat globules - amniotic fluid Gaseous - air - nitrogen Septic - infected material embolise
46
What are some effects of embolism?
Vascular occlusion -> necrosis of target organs -> death Spread of infection (septic emboli) Metastases
47
Where does pulmonary embolism come from?
Comes from venous thrombosis (deep veins of legs, pelvis)
48
Effects of pulmonary embolism
Sudden death Pulmonary necrosis Pulmonary hypertension
49
Why does pulmonary embolism cause sudden death?
Main trunk occlusion -> acute right heart failure
50
Is pulmonary necrosis acute or chronic?
Acute
51
How does pulmonary necrosis come about?
Due to arterial branch occlusion
52
Is pulmonary hypertension acute or chronic?
Chronic
53
How does pulmonary hypertension come about?
Widespread thromboembolic occlusion
54
Consequence of pulmonary hypertension
Right side heart failure
55
What are some special types of embolisms?
Fat Air Amniotic fluid
56
What is the source of a fat embolism?
Bone marrow
57
Causes of fat embolism
Traumatic fracture Soft tissue/MSK injury
58
Pathogenesis of fat embolism
Cause vascular occlusion/damage
59
Are the effects of a fat embolism localised or widespread?
Widespread
60
Alternative name for air embolism
Decompression sickness
61
Signs of decompression sickness and why they happen
Chokes - lungs -> breathless Bends - MSK -> pain Staggers - brain -> loss of balance
62
Pathogenesis for decompression sickness
Nitrogen moves from high pressure in the lungs into the blood (low pressure) Swimming up too quickly does not give nitrogen enough time to leave the blood -> bubbles form -> air bubble ambolise -> DCS
63
Treatment for decompression sickness
Decompression chamber
64
How does amniotic fluid embolism occur?
Amniotic fluid containing dead skin cells of fetus gain access to uterine veins -> embolise
65
When does amniotic fluid embolism occur?
During delivery/abortion
66
What can amniotic fluid embolism progress to?
Acute right heart failure
67
What happens as amniotic fluid embolism progresses?
Material from amniotic fluid trigger coagulation cascade -> disseminated intravascular coagulation (DIVC)
68
Definition of infarction
Necrosis due to ischemia - usually occlusion of artery, sometimes venous drainage
69
Types/colours of infarcts
White infarct - common in solid organs Red infarct - superimposed w/ haemorrhage
70
Diff btw infarction due to arterial occlusion vs venous occlusion and eg for each
Arterial occlusion - wedge shape - eg: renal infarct Venous occlusion - haemorrhage - eg: testicular torsion
71
What are the factors affecting development of an infarct?
Anatomy of arterial blood supply - organs like liver/lungs more resistant as it has dual blood supply Rate of development of vascular occlusion - sudden -> body no chance to react -> more prone to ischemia and necrosis - slow arterial supply -> body can react -> avert significant ischemia Tissue vulnerability - heart and lungs extremely vulnerable to ischemia - tendons resistant to ischemia w/o undergoing necrosis Presence of preexisting hypoxia

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