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Blood > Haemodynamic disorders (disorders of circulation) > Flashcards

Haemodynamic disorders (disorders of circulation) Flashcards

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
Q

What are the consequences of unresolved blood loss?

A

Acute (severe)
- shock

Chronic
- anemia

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26
Q

What is shock?

A

A state of inadequate perfusion and tissue hypoxia due to inadequate cardiac output/effective circulating blood vol

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27
Q

What are the diff types of shock?

A

Hypovolemic shock - due to loss of volume

Cardiogenic shock - pump failure

Septic shock - due to generalised vasodilation
- aka distributive shock

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28
Q

What is the pathophysiology of septic shock?

A

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)

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29
Q

Early signs of shock

A

Skin -> pale and cold

Kidneys -> low uring pdtn

Gut -> bowel stasis

Lung -> tachypnea

Liver -> fatty change

Brain -> reduced conscious level

Heart -> tachycardia

30
Q

What happens as shock progresses?

A

Multi organ fialure

Cyanosis

Necrosis

Coma

31
Q

Protocol for shock

A

Time sensitive

32
Q

What are the vicious cycles of shock?

A

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
Q

What are the factors affecting the prognosis of shock?

A

Type and cause of shock

Prior condition of the pt/co-morbidities

Timeliness and effectiveness of treatment

34
Q

Definition of thrombus

A

An intravascular blood clot formed during life

35
Q

Definition of thrombosis

A

The process in which a thrombus is formed

36
Q

What is Virchow’s triad?

A

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
Q

Pathophysiology of venous thrombosis

A

Stasis -> build up of activated clotting factors -> deep vein thrombosis (DVT) (blood clot in the legs)

38
Q

Where is arterial thrombosis most often seen?

A

In setting of atheromatous disease

39
Q

What are some common clinical states that can lead to thrombosis?

A

Atrial fibrillation

Prosthetic cardiac valves

Post-operative/post-partum state

Prolonged bed rest/immobilisation

Disseminated cancer

Oral contraceptive (oestrogen)

40
Q

Signs of local vascular occlusion

A

Local swelling

Pain

41
Q

What is embolization?

A

Thrombus travels elsewhere and cause vascular occlusion

42
Q

What is the clinical significance of thrombosis in arteries?

A

Thrombus in artery -> arterial occlusion -> ischemia

43
Q

What are some possible outcomes of a thrombus?

A

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
Q

What is an embolus?

A

A detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin

45
Q

Types of thrombus and some eg

A

Solid
- detached thrombus
- tissue fragments

Liquid
- fat globules
- amniotic fluid

Gaseous
- air
- nitrogen

Septic
- infected material embolise

46
Q

What are some effects of embolism?

A

Vascular occlusion -> necrosis of target organs -> death

Spread of infection (septic emboli)

Metastases

47
Q

Where does pulmonary embolism come from?

A

Comes from venous thrombosis (deep veins of legs, pelvis)

48
Q

Effects of pulmonary embolism

A

Sudden death

Pulmonary necrosis

Pulmonary hypertension

49
Q

Why does pulmonary embolism cause sudden death?

A

Main trunk occlusion -> acute right heart failure

50
Q

Is pulmonary necrosis acute or chronic?

A

Acute

51
Q

How does pulmonary necrosis come about?

A

Due to arterial branch occlusion

52
Q

Is pulmonary hypertension acute or chronic?

A

Chronic

53
Q

How does pulmonary hypertension come about?

A

Widespread thromboembolic occlusion

54
Q

Consequence of pulmonary hypertension

A

Right side heart failure

55
Q

What are some special types of embolisms?

A

Fat

Air

Amniotic fluid

56
Q

What is the source of a fat embolism?

A

Bone marrow

57
Q

Causes of fat embolism

A

Traumatic fracture

Soft tissue/MSK injury

58
Q

Pathogenesis of fat embolism

A

Cause vascular occlusion/damage

59
Q

Are the effects of a fat embolism localised or widespread?

A

Widespread

60
Q

Alternative name for air embolism

A

Decompression sickness

61
Q

Signs of decompression sickness and why they happen

A

Chokes
- lungs -> breathless

Bends
- MSK -> pain

Staggers
- brain -> loss of balance

62
Q

Pathogenesis for decompression sickness

A

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
Q

Treatment for decompression sickness

A

Decompression chamber

64
Q

How does amniotic fluid embolism occur?

A

Amniotic fluid containing dead skin cells of fetus gain access to uterine veins -> embolise

65
Q

When does amniotic fluid embolism occur?

A

During delivery/abortion

66
Q

What can amniotic fluid embolism progress to?

A

Acute right heart failure

67
Q

What happens as amniotic fluid embolism progresses?

A

Material from amniotic fluid trigger coagulation cascade -> disseminated intravascular coagulation (DIVC)

68
Q

Definition of infarction

A

Necrosis due to ischemia
- usually occlusion of artery, sometimes venous drainage

69
Q

Types/colours of infarcts

A

White infarct
- common in solid organs

Red infarct
- superimposed w/ haemorrhage

70
Q

Diff btw infarction due to arterial occlusion vs venous occlusion and eg for each

A

Arterial occlusion
- wedge shape
- eg: renal infarct

Venous occlusion
- haemorrhage
- eg: testicular torsion

71
Q

What are the factors affecting development of an infarct?

A

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

Blood (9 decks)

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