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Haematology > Haemodynamic Disorders > Flashcards

Haemodynamic Disorders Flashcards

1
Q

What is the difference between hyperaemia and congestion?

A

Hyperaemia:
- arterial vasodilation
- can be physiological (eg. blushing, muscles in exertion) or pathological (eg. acute inflammation, hypersensitivity)

Congestion (passive hyperaemia):
- venous outflow obstruction
- always pathological (eg. DVT, congestive heart failure)

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2
Q

Which is associated with localised redness and swelling, hyperaemia or congestion?

A

Hyperaemia

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3
Q

Which is associated with oedema and cyanosis, hyperaemia or congestion?

A

Congestion

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4
Q

Which is associated with firm and heavy gross anatomy, hyperaemia or congestion?

A

Congested organs

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5
Q

What are some causes of transudative oedema?

A

Excessive extravascular accumulation of fluid due to changes in Starling´s forces/vascular permeability:
1) increased vascular hydrostatic pressure
2) decreased vascular oncotic pressure
3) increased endothelial permeability
4) lymphatic obstruction
5) Na+/water retention

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6
Q

What are the 2 types of oedematous fluids?

A

Exudate and transudate

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7
Q

What are 4 differences between exudate and transudate?

A

1) Protein content: High in exudate; as in plasma + fibrinogen (albumin w/o fibrinogen in transudate)
2) specific gravity: exudate>transudate
3) Inflammatory cells: exudate>transudate
4) Cause: inflammation vs Starling´s forces

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8
Q

What are 3 causes of localised oedema?

A

1) Venous impairment (eg. venous occlusion)
2) Increased vascular permeability/hyperaemia (eg. inflammation)
3) Lymphatic obstruction/destruction of lymphatics (eg. filariasis/elephantiasis, cancer)

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9
Q

What are 3 causes of generalised oedema?

A

1) Cardiac
- LHF: pulmonary oedema
- RHF: pitting oedema in lower limbs

2) Renal (Nephrotic syndrome)
- glomerular disease -> protein loss
-> decreased vascular oncotic pressure -> fluid extravasation
-> RAA system active -> Na+/H2O retention

3) Hepatic

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10
Q

What are 4 causes of haemorrhage?

A

1) Trauma
2) Abnormal vessels
3) Thrombocytopenia/thrombocytopathies
4) Coagulation factor deficiency (eg. FVIII: hemoarthrosis)

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11
Q

What are the 3 stages in the body´s response to blood loss?

A

1) Initial
- maintenance of BP & flow
- sympathetic activation (initial only, suppressed after hypotension)
- catecholamines release from adrenal medulla

2) Compensation for volume loss
- fluid retention (aldosterone, ADH)
- Redistribution of flow to vital organs

3) RBC replacement

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12
Q

What is the consequence of unresolved, acute and severe blood loss?

A

Shock

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13
Q

What is the consequence of unresolved chronic blood loss?

A

Anaemia

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14
Q

What is shock?

A

A state of inadequate perfusion & tissue hypoxia
(mainly due to inadequate (i) cardiac output (ii) circulating blood volume)

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15
Q

What are the 3 types of shock?
(by cause)

A

1) Hypovolemic shock (eg. haemorrhage, severe burns, vomitting/diarrhoea)

2) Cardiogenic shock (eg. pump failure, AMI)

3) Septic shock “distributive shock” (eg. anaphylactic, neurogenic shock)

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16
Q

What is the pathophysiology of septic shock?

A

Microbial Ags bind to macrophage receptors -> release cytokines:
1) Vasodilation
2) Decreased cardiac contractability
3) Endothelial cell activation
4) Disseminated Intravascular coagulation (DIC)

17
Q

Why is shock treatment time-sensitive?

A

Clinical manifestations can quickly progress to MOF
(golden hour for BC/AC/ATLS)

18
Q

How can shock worsen in a cycle?

A

1) Cardiac (myocardial dmg -> HF)
2 ) Liver (decreased lactate metabolism -> acidosis -> CVS dysf(x))
3) GIT (Mucosal dmg -> decreased fluid + microbe liberation)
4) Kidney (renal failure -> acidosis -> CVS dysf(x))
5) Lung (alveolar dmg -> decreased oxygenation)

19
Q

What are 3 prognosis factors for a px with shock?

A

1) Type/cause
2) Prior & Co-morbidities
3) Timeliness and effectiveness of treatment

20
Q

What is a thrombus?

A

A intravascular blood clot

21
Q

The 3 factors affecting the risk of thrombosis collectively known as _______ and are ______.

A

Virchow´s triad
1) Stasis
2) Endothelial dmg
3) Hypercoagulability

22
Q

What is the main pathogenesis of venous thrombosis?

A

Stasis + accumulation of activated clotting factors

23
Q

What is the biggest risk/concern of venous thrombosis?

A

Embolisation -> distal vascular occlusion
(eg. DVT -> pulmonary artery)

24
Q

What is the main cause of arterial thrombosis?

A

Atheromatous disease (atherosclerosis)

25
Q

What are the 4 possible fates of a thrombus?

A

1) Resolution/lysis
2) Propagation (enlargement of thrombus can lead to occlusion)
3) Organisation & Recanalisation (organised into vessel wall and lumen continuity maintained by vascular recanalisation)
4) Embolism

26
Q

What is an embolus?

A

A detached intravascular solid, liquid, gaseous mass carried by blood to site distant from origin

27
Q

What are the different types of embolism and some examples for each?

A

1) Solid
- thromboemboli
- tissue/tumour fragments
- foreign bodies

2) Liquid
- fat globules
- amniotic fluid

3) Gaseous
- air
- nitrogen

28
Q

What are the possible effects of embolisms?

A

1) Vascular occlusion -> necrosis
2) Septic emboli -> spread of infection
3) Tumour dissemination -> metastasis

29
Q

What are the causes and effects of pulmonary thromboembolisms?

A

Cause: Venous thrombosis (eg. DVT in legs/pelvis)

Effects:
1) Sudden death (main truck occlusion: R HF)
2) Pulmonary necrosis (arterial branch occlusion)
3) Pulmonary hypertension (repeated, chronic, widespread, thromboembolic occlusion)

30
Q

What are the causes and effects of fat embolism?

A

Causes:
- traumatic fracture
- soft tissue/MSK injury

Effects:
- vascular occlusion/dmg
- widespread effects

31
Q

What is amniotic fluid embolism and what are its effects?

A

Rate obstetric complication

Effects:
- Acute R HF
- Disseminated Intravascular Coagulation (DIC)

32
Q

How does decompression sickness lead to air embolism?

A

As a person descends deeper into water, the high pressure forces nitrogen in the lungs into blood (low pressure)

Swimming up too quickly does not give enough time for Nitrogen to return to the lung to be breathed out, instead forming bubbles (air embolism)

33
Q

What are the “chokes”, “bends”, and “staggers” of decompression sickness?

A

“chokes”: breathless (lack of air entering lungs)
“bends”: pain (air embolism in MSK)
“staggers”: loss of balance (air embolism in brain)

34
Q

What is an infarction?

A

Necrosis due to Ischaemia

35
Q

What are the differences between the 2 types of infarcts?

A

White infarcts:
- coagulative necrosis
- arterial occlusion
- single blood supply

Red infarcts:
- haemorrhagic necrosis
- arterial/venous occlusion or reperfusion
- dual blood supply

36
Q

What are the 2 different types of infarcts?

A

Red and white

37
Q

What are 4 factors that influence infarct development?

A

1) Anatomy of arterial blood supply
2) Rate of vascular occlusion development
3) Tissue vulnerability
4) Pre-existing hypoxia

Haematology (9 decks)

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