2 Haemodynamic Disorders Flashcards
*Q: Define oedema.
A: an abnormal increase in interstitial fluid
*Q: What causes oedema? What are are the 3 forces involved?
A: due to fluid movement from plasma to interstitium - occurs when capillary hydrostatic pressure > plasma oncotic pressure + tissue hydrostatic pressure
3 forces involved:
Capillary hydrostatic pressure- pushing out of vessel
Plasma oncotic pressure- pulling in to vessel
Tissue hydrostatic pressure- pushing into vessel
Q: What is oncotic pressure?
A: pressure exerted by plasma protein
*Q: What are the 4 causes of oedema? Describe them with examples.
A: Increased Capillary Hydrostatic Pressure: E.g. venous obstruction, congestive cardiac failure
Decreases Capillary Oncotic Pressure: E.g. nephrotic syndrome (loss of proteins through leaky kidneys), cirrhosis, malnutrition
Inflammation: Increased vascular permeability facilitates movement of fluid into the interstitium
Lymphatic Obstruction: lymphoedema = build up of fluid caused by damaged lymph vessels (potential side effect of breast cancer treatment)
Filariasis can cause massive lymphatic obstruction
*Q: What is pulmonary oedema and what can it be? (2)
A: fluid build up in lungs
can be acute or chronic
*Q: What are the 2 types of pulmonary oedema and how do they arise?
A: Cardiogenic Pulmonary Oedema: left ventricular failure -> increased pressure in the left atrium -> raised hydrostatic pressure in the pulmonary capillary bed -> fluid accumulates in the interstitial space and then spills over into the alveolar spaces (pressure)
Non-Cardiogenic Pulmonary Oedema: caused by increase in permeability of the normal alveolar-capillary barrier (permeability)
Q: What is ARDS? (2) Commonly seen? Common causes? (3)
A: Acute Respiratory Distress Syndrome
what non-cardiogenic pulmonary oedema is known as
commonly seen in injecting drug users
Most Common causes of ARDS: Sepsis, Shock and Trauma
Q: What is the main symptom of a pulmonary oedema? What makes it worse?
A: Dyspnoea
worse when they lie flat because of the movement of fluid (this is called orthopnoea)
Q: What can fluid collection in alveolar spaces lead to?
A: predisposes to bacterial infection in the lung (pneumonia)
*Q: What is a cerebral oedema? What does it contribute to? (2) What can it lead to? (4)
A: fluid build up in brain (swelling)
Cerebral oedema contributes to a rise in intracranial pressure (ICP) =
High ICP can lead to brain herniation (squeezing of the brain across a structure within the skull)
and death
Leads to confusion, nausea and vomiting
*Q: What is generalised oedema? What is severe generalised oedema called?
A: widespread accumulation of fluid is subcutaneous tissues and serous cavities
anasarca
*Q: How does heart failure causing oedema? Describe its mechanism.
A: Low Renal Blood Flow -> Release of Renin from kidneys -> Formation of angiotensin II -> Release of aldosterone from adrenal gland -> Absorption of sodium and water from kidneys -> Generalised oedema
*Q: What are the consequences of oedema in a peripheral setting?
A: Impaired wound healing - Patients with generalised oedema are more prone to getting cellulitis
*Q: Define thrombosis.
A: Abnormal blood clot formation in the circulatory system
*Q: What are the 3 causes of thrombosis.
A: Vessel wall injury, stasis (alteration to blood flow), hypercoagulability
*Q: How can vessel wall injury cause thrombosis? 2 methods.
A: Physical Damage to Endothelium - exposes ECM and activated blood clotting cascade
Endothelial Dysfunction - endothelium isn’t working normally so causes alteration in the formation of pro-coagulants and anti-coagulants
*Q: How can stasis cause thrombosis?
A: Normal Blood Flow - platelets are usually found in the centre of the vessel
Stasis - loss or normal flow - platelets are exposed to the endothelium - more likely to form a clot
Stasis can also cause thrombosis by changing the dilution of blood clotting factors
*Q: What can cause hypercoagulabilty? (2)
A: Primary - Genetic Disorder - patients are more likely to form blood clots - Most common hypercoagulability disorder in UK - Factor V Leiden
Secondary - Acquired - risk factors for developing thrombosis - obesity, neoplasia, oral contraceptive pill
*Q: What can cardiac thrombosis be caused by? Include what causes 2 examples of it.
A: stasis
Left Atrial Thrombosis is usually related to atrial fibrillation
Left Ventricular Thrombosis is usually related to prior myocardial infarction
*Q: What is the most common complication of cardiac thrombosis?
A: Systemic Embolisation
*Q: What is arterial thrombosis? What can cause it?
A: blood clot in an artery
usually related to vessel wall injury = often caused by atherosclerotic plaques
*Q: What can arterial thrombosis lead to?
A: Stenosis = narrowing of the artery by the thrombus
Stenosis causes ischaemia of the tissue supplied by the artery
Occlusion = complete blockage of the artery by the thrombus -> causes infarction of the tissue supplied by the artery
*Q: What is venous thrombosis and what are key factors? Where do most form?
A: blood clot in vein
stasis and hypercoagulability
most form in DEEP VEINS (DVT)
Q: What are the risk factors of venous thrombosis formation? (5)
A: age, obesity, malignancy, immobility, oral contraceptive pill
*Q: What is the most common complication of venous thrombosis?
A: Pulmonary embolism
*Q: What are the 4 fates of a thrombus?
A: 1. Propagation- gets larger by accumulates more fibrin
- Embolisation- dislodges and travels to distant site
- Dissolution- destroyed by fibrinolytics (can be endogenous or given as a drug)
- Organisation and Recanalisation- As a result of the thrombus, there is inflammation -> Thrombus becomes fibrotic and remodels -> Lumen appears again allowing blood flow
*Q: Define embolism. What material is it made from?
A: detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin
Most emboli are fragments of dislodged thrombus (thromboemboli) but embolic material can be Fat,
Air, Amniotic Fluid, Tumour
*Q: What is the most significant consequence of venous thromboembolism?
A: pulmonary (thrombo)embolism
*Q: What does the consequence of a pulmonary embolism depend on? (2) Give examples and include what the consequences are. (4)
A: depends on the size of the embolus and where it gets lodged.
Emboli lodging in a major pulmonary artery can cause instantaneous death
If it gets lodged at the bifurcation of one pulmonary artery into two, it is called a saddle embolus
Emboli lodging in medium sized arteries present with breathlessness
Small emboli lodging in small arteries cause non-specific symptoms - e.g. dizziness, chest pain, breathlessness
*Q: Define haemorrhage.
A: Extravasation of blood due to vessel rupture.
*Q: What can cause a haemorrhage? (3)
A: Trauma, intrinsic disease of the vessel, Rupture of a major vessel causes acute haemorrhage
*Q: What does the result of a haemorrhage depend on? (3)
A: Volume and rate of haemorrhage, Site
Q: Why is the formation of a solid haematoma within the cranial cavity fatal? (3)
A: causing a RISE IN INTRACRANIAL PRESSURE and TONSILLAR HERNIATION = pushing the cerebellar tonsils through the foramen magnum possibly causing compression of the lower brain stem
*Q: Define shock. When does it occur and how? What is it characterised by?
A: an acute medical condition associated with a fall in blood pressure
occurs when tissue perfusion is insufficient to meet metabolic requirements.
Characterised by HYPOTENSION
Prolonged hypotension causes circulatory collapse leading to ischaemia of multiple organs
*Q: What are the 5 types of shock?
A: 1. Hypovolaemic:
- Cardiogenic:
- Septic:
- Anaphylactic:
- Neurogenic:
*Q: Define infarction.
A: Tissue necrosis due to ischaemia
*Q: What can cause infarctions? (3)
A: Most due to obstruction of an artery
Some may occur due to venous obstruction
More rarely occurs due to vasospasm and compression
Q: What are factors influencing development of infarction? (4)
A: Nature of Blood Supply - Kidney and spleen are more susceptible to infarction as they are end organs with a single blood supply
Rate of Development of Occlusion- If the occlusion develops slowly, there could be enough time to provide an alternate blood supply
Vulnerability to Hypoxia - neurones are very susceptible to hypoxia
Oxygen content of the blood- reduced levels of oxygen in their blood = prone to developing infarction
Q: What is atherosclerosis? What does it affect? Develops? Types? (2)
A: Complex chronic disease of plaque build up inside arteries
Affects medium and large vessels
Develops from fatty streak into plaque within the intima (innermost layer of blood vessel)
can get stable and unstable plaque (more likely to rupture)
Q: What is the process of atherosclerosis?
A: Endothelial damage -> Macrophage infiltration - macrophages release cytokines -> Cytokines recruit LDLs -> LDLs become oxidised -> Oxidised LDLs are pro-inflammatory and drive progression of plaque -> Smooth muscle cells migrate from the tunica media to the lesion -> Smooth muscle cells deposit a collagen rich matrix that forms a protective fibrous cap
Q: What is the cause of hypovolaemic shock? (2) What are the consequences? (5)
A: Trauma, Haemorrhage -> loss of blood -> Low stroke volume SV –> Reduced cardiac output CO -> Reduced mean arterial pressure MAP-> Body tries to compensate with tachycardia
Q: What is the cause of cardiogenic shock? (2) What are the consequences? (3)
A: Acute MI, Cardiac Tamponade -> IMPAIRED CARDIAC FUNCTION
Cardiac Tamponade = accumulation of fluid in the pericardium resulting in compression of the heart =
Heart isn’t working properly so SV
Q: What is the cause of septic shock? (2) What are the consequences? (2)
A: Vasodilation as a result INFLAMMATORY RESPONSE -> Reduced systemic vascular resistance SVR -> Reduced MAP
Q: What is the cause of anaphylactic shock? (2) What are the consequences? (2)
A: Vasodilation, Increased Permeability -> Result of IgE MEDIATED HYPERSENSITIVITY -> Reduced SVR -> Reduced MAP
Q: What is the cause of neurogenic shock? What are the consequences? (2) When does it normally happen? (2)
A: loss of vasomotor tone - causes widespread vasodilation and reduced SVR -> Normally happens after trauma which results in INJURY TO THE SYMPATHETIC PATHWAYS + in neurogenic shock, you’ve disrupted the sympathetic pathways so you won’t be able to become tachycardic to increase cardiac output
