Haemodynamic disorders Flashcards

Oedema: recall the aetiological classification of oedema, and explain the possible consequences of oedema at different sites Thrombosis, embolism and infarction: define thrombosis, embolism and infarction; recall the causes and possible consequences of each Haemorrhage: list causes and possible consequences of haemorrhage Shock: define shock and identify possible causes and mechanisms

1
Q

What is odema?

A

An abnormal increase in interstitial fluid. Fluid that bathes tissues and surrounds cells.
Hydrostatic pressure pushing the fluid out is greater than the osmotic pressure pulling it in.

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2
Q

What are the three forces involved in oedema?

A

Capillary hydrostatic pressure pushing fluid out.
Plasma oncotic pressure pulling fluid in.
TISSUE hydrostatic pressure pushing fluid INTO vessels.

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3
Q

What is the definition of aetiology?

A

Causes of a disease.

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4
Q

What are the aetiologies of oedema? (x5)

A

Increased capillary hydrostatic pressure: occurs when impaired venous return or increased venous pressure e.g. in heart failure.
Salt and H2O retention: tissues retain H2O – this is usually because of high salt intake. Indicated by high hydrostatic pressure.
Reduced plasma oncotic pressure: malnutrition and reduced albumin in blood.
Inflammation: could be caused by sepsis or localised cellulitis (infection deep in skin). Inflammation results in increased blood vessel wall permeability which facilitates movement of fluid into interstitium.
Lymphatic obstruction: leads to accumulation in interstitial space. Maybe from lymphatic vessel damage.

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5
Q

What is oedema called when lymphatic obstruction is the cause?

A

Lymphoedema.

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6
Q

What are the two types of oedema?

A

Generalised and Localised.

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7
Q

What is generalised oedema? How can it be identified? What is that oedema called?

A

Widespread accumulation of fluid in subcutaneous tissues and serious cavities (pleural, pericardial or peritoneal).
In subcutaneous tissue, lower limbs can be seen to be particularly affected because gravity effects more greatly. When pressed = produces an indentation –> called generalised PITTED oedema.

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8
Q

What is generalised oedema commonly caused by? (x4) Explain what happens in heart failure.

A
Heart failure (specifically Left Ventricular Failure) = systemic blood accumulation. Blood stops pumping do blood accumulates in areas affected by gravity = dependent oedema.  
Inflammation e.g. sepsis 
Venous hypertension (means increased hydrostatic pressure and lesser ability of venous return). 
Lymphatic obstruction.
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9
Q

What is localised oedema?

A

Oedema that affects specific areas. Not systemic.

Commonly pulmonary and cerebral oedema.

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10
Q

What are the two causes of pulmonary oedema?

A

Usually from left heart failure - causes increased pressure in left atrium which causes back pressure in pulmonary capillaries = Increased hydrostatic pressure in the pulmonary capillary bed.
So fluid pushed out and accumulates in the interstitial space and eventually into the aveolar spaces.
OR, can be caused by increased permeability from sepsis or shock.

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11
Q

What are the consequences of pulmonary oedema? (x3)

A

Dyspnoea (breathlessness).
Worse when lying flat!
Fluid in alveoli predisposes to bacterial infection in the lungs e.g. pneumonia.

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12
Q

What are the four types of cerebral oedema?

A

Vasogenic cerebral oedema – physical breakdown of blood-brain barrier caused by trauma or tumours which release factors that break down the barrier.
OR Cytotoxic cerebral oedema – derangement of the Na+/K+ pump increases sodium concentration inside cells which encourages water take-up by such cells –> swelling.
OR Osmotic – reduced osmotic osmolality (less solutes in the blood).
OR Interstitial – caused by rupture of CSF-brain barrier. CSF = cerebrospinal fluid.

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13
Q

What are the consequences of cerebral oedema? (x4)

A

Increased intracranial pressure (pressure in skull).
Leads to brain herniation.
Confusion, vomiting.

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14
Q

What is thrombosis?

A

Abnormal blood clot formation in the circulatory system.

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15
Q

What are the three causes?

A

Vessel wall damage.
Stasis (alteration to blood flow).
Hypercoagulability (abnormality in blood coagulation – more likely to form blood clots)

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16
Q

What happens in vessel wall damage that causes thrombosis? (x2)

A

Damage to endothelium exposes ECM and activates blood clotting cascade.
OR, Endothelium isn’t working properly.

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17
Q

What happens stasis that causes thrombosis? (x2)

A

Loss of normal flow means platelets are exposed to endothelium (they would usually found in centre of the vessel not near endothelium) so MORE LIKELY to form a clot.
Stasis can change the dilution of blood clotting factors.

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18
Q

What happens in hypercoagulability to cause thrombosis? (x2)

A

Genetic disorder – primary cause.

Acquired cause e.g. obesity or oral contraceptive which are RISK FACTORS – secondary cause.

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19
Q

What are the two types of thrombosis?

A

Venous and arterial.

20
Q

What are the most common causes venous thrombosis? (x2)

A

Stasis and hypercoagulability.

21
Q

Where is venous thrombosis usually found?

A

Deep leg veins e.g. DVT.

22
Q

What causes arterial thrombosis?

A

Injury to blood vessel almost always. Caused by atherosclerotic plaques (accumulation of cholesterol and fat).

23
Q

What are the two consequences of arterial thrombosis?

A

STENOSIS: narrowing of artery by the thrombus = ISCHAEMIA of the tissue supplied by the artery.
OCCLUSION: complete blockage of the artery by the thrombus = INFARCTION of the tissue supplied by the artery.

24
Q

Four fates of the thrombus?

A

Propagation – thrombus gets bigger.
Embolization – dislodges and travels to distant site.
Dissolution – thrombus destroyed by fibrinolytics (can be endogenous (have internal cause) or given as a drug).
Organisation and recanalization – thrombus causes inflammation, thrombus becomes fibrotic and remodels, and lumen appears again allowing blood flow.

25
Q

What material could the emboli be? (x5)

A

Blood clot.

Fat (if you break a long bone), air (from injection), amniotic fluid, tumour.

26
Q

Why are embolisms dangerous?

A

Can lodge in vessels and block them off!

27
Q

What is an infarct?

A

An area of ischemic necrosis (tissue death from restricted blood supply) caused by occlusion (blockage of blood vessel). It is not the actual blockage of a blood vessel, it’s the tissue necrosis.
Mostly due to arterial obstruction.

28
Q

What are the consequences of infarction? (x2 points)

A

Infarcts heal by repair.

Although structural integrity is maintained, there is permanent loss of functional tissue.

29
Q

What are the two types of infarct? Main cause of each?

A

Red infarct – HAEMORRHAGIC and affects organs with dual blood supply. Caused mostly by venous occlusion.
White infarct – ANAEMIC and affects solid organs which have one blood supply. Caused by arterial occlusion.

30
Q

What is a venous thromboembolism?

A

Blood clot forms most often in deep veins of leg, groin or arm (DVT) and travels in the circulation, lodging in the lungs as a pulmonary (thrombo)embolism.

31
Q

What is a pulmonary thromboembolism? What is the symptom range?

A

Emboli lodging in a pulmonary artery.
Small emboli lodging (in peripheral pulmonary artery) = breathlessness, chest pain, dizziness.
Large emboli lodging (in major pulmonary artery) = instantaneous death.

32
Q

What is a haemorrhage?

A

Extravasation (leakage) of blood due to vessel rupture.

Can be external or enclosed within a tissue.

33
Q

What is a haematoma?

A

A localised mass of extravasated blood that is relatively or completely confined within an organ or tissue.

34
Q

Causes of haemorrhage? (x2)

A
Trauma 
Intrinsic disease (caused by internal factors) of the vessel.
35
Q

What is the consequence of an acute haemorrhage? (x3)

A

Hypovolaemia (decreased volume of circulating blood in the body).
Shock
Death

36
Q

When can a SMALL haemorrhage become problematic?

A

When it affects a vital site. For example, brainstem haemorrhage. Even a small bleed can increase pressure enough on the brain tissue to cut off blood supply.

37
Q

What is shock?

A

Occurs when tissue perfusion (passage of blood through tissue) is insufficient to meet metabolic requirements.

38
Q

Causes of shock?

A

HYPOTENSION.

39
Q

Consequence of shock? (x3)

A

Circulatory collapse where circulation fails to maintain supply of oxygen to tissues. Leads to ischaemia.
Most vulnerable organs are kidneys, brain, lungs.
MULTIPLE ORGAN FAILURE and tissue death.

40
Q

Types of shock? (x5)

A

Hypovolaemic, Cardiogenic, Septic, Anaphylactic, Neurogenic.

41
Q

What is hypovolaemic shock?

A

Caused by loss of blood volume.
Results in reduced cardiac output (volume pumped by heart) and lower arterial pressure.
Body tries to compensate with tachycardia.

42
Q

What is cardiogenic shock?

A

Caused by impaired cardiac function.
Caused by heart attack OR compression of the heart by build up of fluid in the pericardium.
Because heart isn’t working properly, heart cannot pump enough blood, hence low blood pressure and SHOCK.

43
Q

What is septic shock?

A

Result of inflammatory response from bacterial infection. This causes vasodilation and dangerously low blood pressure = shock.

44
Q

What is anaphylactic shock?

A

Result of Immunoglobulin E (antibody) mediated hypersensitivity. Causes vasodilation and increased blood vessel permeability = low blood pressure.

45
Q

What is neurogenic shock? (x2 points)

A

Caused by trauma.
Results in injury to sympathetic pathways. Results in loss of vasomotor tone (tension in smooth muscle of blood vessel walls). This causes widespread vasodilation and low blood pressure.
Because you’ve disrupted the sympathetic pathway, you won’t become tachycardic to increase cardiac output.