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Mcd Cell Pathology > 2- Haemodynamic Disorders > Flashcards

2- Haemodynamic Disorders Flashcards

1
Q

What causes fluid to move into tissue

A

Capillary Hydrostatic Pressure - pushing OUT of vessel
• Plasma Oncotic Pressure - pulling IN to vessel
This is the pressure exerted by plasma protein
• Tissue Hydrostatic Pressure - pushing IN to vessel

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2
Q

What causes oedema

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
MOST COMMON - lymphoedema - breast cancer treatment - damage the lymph vessels leading to build up of fluid
Filariasis can cause massive lymphatic obstruction

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3
Q

What is pulmonary oedema

A

Cause: Raised hydrostatic pressure in the pulmonary capillary bed
• Most Common Cause of this: Left Ventricular Failure
increased pressure in the left atrium causes back pressure into the capillaries. This pushes water into the interstitial space
• Fluid accumulates in the interstitial space and then spills over into the alveolar spaces. This is Cardiogenic Pulmonary Oedema
• You can also get Non-Cardiogenic Pulmonary Odema caused by increased permeability
This is known as ARDS (Acute Respiratory Distress Syndrome) Commonly seen in injecting drug users
Most Common causes of ARDS: Sepsis, Shock and Trauma
• Can be chronic or acute
• MAIN SYMPTOM: DYSPNOEA
• Dyspnoea is worse when they lie flat because of the movement of fluid (this is
called orthopnoea)
• Fluid collection in alveolar spaces predisposes to bacterial infection in the lung
(pneumonia)

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4
Q

What are 4 types of cerebral oedema

A
  1. Vasogenic - physical breakdown of blood-brain barrier
    Causes: Trauma and Tumours (by releasing factors which break down
    barriers)
  2. Cytotoxic - derangement of sodium-potassium membrane pump
    Common in ischaemic strokes
    Increase in sodium within cells encourages water to be taken up Causes intracellular oedema
  3. Osmotic - reduction in plasma osmolality
    Cause: SIADH (Syndrome of Inappropriate ADH secretion) SIADH is commonly caused by SMALL CELL LUNG CARCINOMA ADH release –> more water reabsorbed –> decrease in plasma osmolality
  4. Interstitial - breakdown of CSF-brain barrier
    Cause: Obstructive Hydrocephalus (abnormal accumulation of cerebrospinal fluid in the brain - due to blockage in flow of CSF) CSF (NOT blood plasma) moves into the interstitial space
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5
Q

What does cerebral oedema cause

A

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
• Strategies to reduce ICP: raise head, inducing dehydration with drugs, surgical
decompression

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6
Q

What is osmolarity and osmololity

A 
OsmolaRity = number of solute particles per LITRE 
OsmolaLity = number of solute particles per KILOGRAM
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7
Q

What is generalised oedema

A

Severe Generalised Oedema = Anasarca
• It is the widespread accumulation of fluid in subcutaneous tissues and serous cavities
• Same causes of localised oedema cause generalised oedema
• Common Causes:
Left Ventricular Failure - dependent oedema (accumulated in areas affected by gravity)
Nephrotic Syndrome - fluid accumulates in all parts of the body

• Consequences of Oedema in peripheral setting:
Impaired wound healing
Patients with generalised oedema are more prone to getting cellulitis

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8
Q

How does heart failure cause oedema

A

Mechanism of Heart Failure causing Oedema:
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

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9
Q

What can happen to a thrombus

A
  1. Propagation
    Thrombus gets BIGGER - accumulates more fibrin and takes up a larger portion of the vessel
  2. Embolisation
    Dislodges and travels to distant site
  3. Dissolution
    Thrombus is destroyed by fibrinolytics (can be endogenous or given as a
    drug)
  4. Organisation and Recanalisation
    As a result of the thrombus, there is inflammation Thrombus becomes fibrotic and remodels
    Lumen appears again allowing blood flow
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10
Q

What is thrombosis and what causes it

A

Abnormal blood clot formation in the circulatory system.
• Vessel Wall Injury
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
• Stasis (alteration to blood flow)
Normal Blood Flow - laminar - platelets
are usually found in the centre of the vessel and is not exposed to endothelium - less chance of thrombosis
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
• Hypercoagulability
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

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11
Q

Describe cardiac thrombosis

A

STASIS is the main way that thromboses form
EXAMPLE: due to Atrial Fibrilation
• Left Atrial Thrombosis is usually related to atrial fibrillation
• Left Ventricular Thrombosis is usually related to prior myocardial infarction
• MOST IMPORTANT COMPLICATION: Systemic Embolisation

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12
Q

Describe arterial thrombosis

A

Almost always related to vessel wall injury
• Vessel wall injury is often caused by atherosclerotic plaques
• 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
• Occlusion causes infarction of the tissue supplied by the artery

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13
Q

Describe venous thrombosis

A 
KEY FACTORS: Stasis and Hypercoagulability
• Risk Factors:
Age
Obesity
Malignancy Immobility
Oral Contraceptive Pill
• Most form in DEEP VEINS (DVT)
• MOST IMPORTANT COMPLICATION: Pulmonary Embolism
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14
Q

What is an embolism

A

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

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15
Q

What are embolisms made from

A 
Most emboli are fragments of dislodged thrombus (thromboemboli)
• Rarer types of embolic material:
Fat
Air
Amniotic Fluid Tumour
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16
Q

What are the types of thromboembolism

A

Venous Thromboembolism
• Most originate in Deep Veins (e.g. DVT)
• Most Significant Consequence - pulmonary (thrombo)embolism

Pulmonary Embolism
Consequence 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
• 30% of patients with PE die from it
• Risk of death INCREASES with time taken to make the diagnosis

Arterial Thromboemboli
• Most originate in CAROTID ARTERIES
• Most likely to affect cerebral arteries - causing STROKE

Cardiac Thromboemboli
• Most originate on the LEFT SIDE OF THE HEART
• May lodge in:
Cerebral Artery - STROKE
Mesenteric Artery - BOWEL INFARCTION
Lower Limb Artery - ACUTE LOWER LIMB ISCHAEMIA

17
Q

Describe haemorrhage

A

CAUSES:
Trauma
Intrinsic disease of the vessel
• Haemorrhage can be external or enclosed within a tissue
• Haematoma = a localised mass of extravasated blood that is relatively or
completely confined within an organ or tissue
• Haemorrhages are classified based on size:
1-2mm = petechiae
>3mm = purpura
1-2cm = ecchymoses
Large accumulations in body cavities (e.g. haemothorax)
• The result of a haemorrhage depends on:
Volume and rate of haemorrhage
Site
• Rupture of a major vessel causes acute haemorrhage with risk of:
Hypovolaemia Shock
Death
• Rupture of a small vessel can still be fatal if it occurs at a vital site - e.g. brainstem haemorrhage
• Formation of a solid haematoma within the cranial cavity can be FATAL by causing a RISE IN INTRACRANIAL PRESSURE and TONSILLAR HERNIATION NOTE: Tonsillar Herniation - pushing the cerebellar tonsils through the foramen magnum possibly causing compression of the lower brain stem
• Chronic Low Grade Haemorrhage
May present with iron deficiency anaemia EXAMPLE: bleeding from colonic carcinoma

18
Q

What are the 5 types of shock

A
  1. Hypovolaemic
    Most commonly due to LOSS OF VOLUME
    CAUSES include: Trauma, Haemorrhage
    Low blood volume –> Low SV –> Reduced CO –> Reduced MAP Body tries to compensate with tachycardia
    By increasing HR you try to maintain regular CO
  2. Cardiogenic
    Due to IMPAIRED CARDIAC FUNCTION
    CAUSES include: Acute MI, Cardiac Tamponade
    Cardiac Tamponade - accumulation of fluid in the pericardium resulting in compression of the heart
    Heart isn’t working properly so SV is REDUCED leading to shock
  3. Septic
    Result of INFLAMMATORY RESPONSE CAUSE: Vasodilation
    Reduced SVR –> Reduced MAP
  4. Anaphylactic
    Result of IgE MEDIATED HYPERSENSITIVITY Similar to Septic Shock
    CAUSES: Vasodilation, Increased Permeability Reduced SVR –> Reduced MAP
  5. Neurogenic
    RARE
    Normally happens after trauma
    Result of INJURY TO THE SYMPATHETIC PATHWAYS
    CAUSES: loss of vasomotor tone - causes widespread vasodilation and reduced SVR
    Also in neurogenic shock, you’ve disrupted the sympathetic pathways so you won’t be able to become tachycardic to increase cardiac output
19
Q

What is shock

A

Occurs when tissue perfusion is insufficient to meet metabolic requirements.
• Characterised by HYPOTENSION
• Prolonged hypotension causes circulatory collapse leading to ischaemia of
multiple organs
• Most Vulnerable Organs: Kidneys, Bowel, Brain, Lungs, Heart

20
Q

What is infarction

A

Tissue necrosis due to ischaemia.
• Most due to obstruction of an artery
• Some may occur due to venous obstruction
• More rarely occurs due to vasospasm and compression
• Red Infarcts - haemorrhagic - affects organs with a dual blood supply - generally
caused by venous blood supply
• White Infarcts - anaemic - affects solid organs which have one blood supply
• Infarcts heal by REPAIR
• Although structural integrity is maintained, there is some permanent loss of
functional tissue

21
Q

What are Factors influencing development of infarction:

A

• Nature of Blood Supply
Lung and Liver = Dual Circulation
Kidney and Spleen = End Organs (single blood supply)
If there is an obstruction in the lung or liver, they can use other vessels to supply the tissue.
Kidney and spleen are more susceptible to infarction
• Rate of Development of Occlusion
If the occlusion develops slowly, there could be enough time for Collateral
Vessels to form and provide an alternate blood supply
• Vulnerability to Hypoxia
EXAMPLE: neurones are very susceptible to hypoxia, fibroblasts aren’t
• Oxygen content of the blood
EXAMPLE: patients who have anaemia and chronic heart failure will have reduced levels of oxygen in their blood - more prone to developing infarctions

22
Q

Scribe myocardial infarction

A

Looks like a wedge shape - apex of the wedge is where the occlusion occurred TWO Types of MI:

Transmural Infarction
• Entire wall is affected
• Occurs when there has been
complete blockage of a vessel and complete cessation of the blood supply
Subendocardial Infarction
• Some myocardial tissue underneath the endocardium has been affected by infarction
• Caused by drop in blood oxygen content or rapid drop in blood supply (e.g. due to blood loss)

23
Q

Describe small bowel infarction

A

RED INFARCT
• Surgical emergency
• Patients present with severe lactic acidosis

24
Q

Describe atherosclerosis

A

Complex chronic disease - underlying cause of most vascular diseases
• Focal intimal accumulation of lipids and fibrous tissue associated with smooth
muscle proliferation
• Affects medium and large vessels
• Develops from fatty streak into plaque within the intima

25
Q

What is the process of atherosclerosis?

A
  1. Endothelial damage
  2. Macrophage infiltration - macrophages release cytokines
  3. Cytokines recruit LDLs
  4. LDLs become oxidised
  5. Oxidised LDLs are pro-inflammatory and drive progression of plaque
  6. Smooth muscle cells migrate from the tunica media to the lesion
  7. Smooth muscle cells deposit a collagen rich matrix that forms a protective
    fibrous cap
26
Q

What are 2 types of plaque?

A 
Stable Plaque
Less inflammation
Well developed thick fibrous caps Slow growing
Less likely to rupture
• Unstable Plaque
More inflammation
Lipid rich necrotic core Thin fibrous cap
MORE LIKELY TO RUPTURE
27
Q

What can hypokalaemia cause

A

Shock. It is hypokalaemia (low blood potassium), not hyperkalaemia (high blood potassium), that usually causes shock.

Mcd Cell Pathology (6 decks)

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