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MCD - cell pathology > Haemodynamic disorders > Flashcards

Haemodynamic disorders Flashcards

1
Q

What is oedema?

A

An abnormal increase in interstitial fluid

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2
Q

Under normal circustances, how does fluid leave the circulation at the arterial end?

A

Hydrostatic pressure > oncotic pressure

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3
Q

Under normal circustances, how does fluid leave the circulation at the venous end?

A

Oncotic pressure > hydrostatic pressure

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4
Q

What is the flow of interstitial fluid governed by?

A
  1. Hydrostatic and oncotic pressures
  2. Endothelial permeabillity
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5
Q

Name 5 aetiologies of oedema

A
  1. Increased hydrostatic pressure
    • Heart failure results in increase in hydrostatic pressure (generalised oedema)
  2. Salt and H₂O retention
    • Reduced cardiac output stimulates renin-angiotensin system which leads to sodium retention (generalised oedema)
  3. Reduced plasma oncotic pressure (reduced albumin)
    • Plasma oncotic pressure is governed by [albumin]
    • When [albumin] < 25g/L fluid leaves microcirculation
    • Cause of generalised oedema
    • Loss of protein (nephrotic syndrome, protein loos enteropathy)
  4. Inflammation
    • Loss of protein rich fluid locally
  5. Lymphatic obstruction
    • Localised oedema
    • Non pitting protein rich oedema
    • Obstruction by tumour, lymph node dissection, chronic inflammation
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6
Q

What is the difference between localised and generalised oedema?

A

LOCALISED = cerebral and pulmonary oedema

GENERALISED = fluid in serous cavities (pleural, pericardial, peritoneal) > 5L

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7
Q

What are the causes of localised oedema?

A
  • Left heart failure
  • Inflammation
  • Venous hypertension
  • Lymphatic obstruction
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8
Q

What are the causes of generalised oedema?

A
  • Congestive heart failure
  • Hypoproteinaemia (low protein content)
  • Nutritional oedema
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9
Q

What happens during pulmonary oedema?

A
  • Normally plasma oncotic pressure > hydrostatic pressure in pulmonary capillaries
  • Left heart failure increases hydrostatic pressure in pulmonary capillary bed
  • Fluid accumulates first in interstitial space and then eventually spills into alveolar spaces
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10
Q

What are the signs and symptoms of pulmonary oedema?

A
  • Breathelessness (dyspnoea)
  • Breathlessness typically worse on lying flat (orthopnoea)
  • Fluid in alveolar spaces predisposese to bacterial infection in lung (pnuemonia)
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11
Q

What is thrombosis?

A

Abnormal blood clot formation in the circulatory system

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12
Q

According to Virchow’s Triad, what are the three causes of thrombosis?

A
  1. Endothelial injury (usually where vessels bifurcate)
    • –> platelet activation
    • Arteries have high rates of blood flow and hence are under high shear stress
  2. Stasis or turbulent blood flow
    • –> endothelial injury
    • Stasis = disruption of laminar blood flow and development of venous thrombi
    • Turbulent = endothelial injury and formation of local pockets of stasis –> arterial and cardiac thrombi
  3. Blood hypercoagulability (can be genetic or acquired)
    • Blood disorder
    • Can be primary or secondary
    • Primary = factor V mutation, protein C deficiency
    • Secondary = multifactorial, obesity, cancer, stasis, advancing age, use of oral contraceptive pill
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13
Q

What is venous thrombosis caused by?

A

Usually stasis and hypercoagulability

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14
Q

TRUE OR FALSE:

Most venous thromboses form in deep leg veins

A

TRUE

E.g. deep venous thrombosis (DVT)

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15
Q

What is the most important potential complication of venous thrombosis?

A

Pulmonary embolism

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16
Q

What is arterial thrombosis caused by?

A

Almost always related to vessel wall injury caused by atherosclerotic plaques

17
Q

What are the complications of arterial thrombosis?

A
  • Narrowing (stenosis) of artery by thrombus causes ischaemia of the tissue supplied by the artery
  • Complete blockage (occlusion) of artery causes infarction of the tissue supplied by the artery
18
Q

What are the 4 fates of thrombi?

A
  1. Propagation
    • Accumulation of further platelets and fibirin in a semi-occlusive thrombus
  2. Embolisation
    • Thrombi dislodge and travel through circulation
  3. Dissolution
    • Fibrinolysis in early thrombi
  4. Organisation and recanalisation
    • Older thrombi enveloped by fibroblasts, endotheilal cells and smooth muscle cells
    • Capillary channels develop within thrombus
19
Q

What is the clinical significance of thrombosis?

A

Come to clinical attention when they:

  • either obstruct arteries or veins
  • when they embolism
20
Q

What are emboli?

A

Abnormal material within the circulatory system that is carried in the blood to a site distant from its point of origin.

Most emobli are fragments of dislodged thrombus (thromboemboli)

Other rarer types include fat, air, amniotic fluid, tumour

21
Q

What are infarcts?

A

Areas of ischaemic necrosis caused by occlusion

22
Q

What is infarction most commonly caused by?

A

Thrombic or embolic vascular occlusion (though other causes need to be excluded)

23
Q

What are the differences between red and white infarcts?

A

RED INFARCTS:

  • Occur as a result of venous occlusion
  • Occur in loose tissue (e.g. lungs)
  • Occur in organs with dual circulation (e.g. lung, bowel)
  • Can reperfuse a site of previous arterial occlusion

WHITE INFARCTS:

  • Occurs as a result of arterial occlusion
  • In dense/solid organs
24
Q

TRUE OR FALSE:

Infarcts heal by repair meaning that both structural integrity and function are maintained

A

FALSE:

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

25
Q

What are pulmonary emboli?

A
  • Originate from deep vein thrombosis (lower extremities)
  • Can range form silent to symptomatic and even lead to sudden death
26
Q

What are systemic emboli?

A
  • Arise in the arterial system
  • Originate from:
    • dislodged atheromatous
    • thrombi from within heart
  • Thrombi within the heart:
    • due to cardiomyocyte death and thus no contractility
    • due to atrial fibrillation
27
Q

What is myocardial infarction caused by?

A

Most commonly coronary artery occlusion:

  • Occlusive thrombus in coronary artery
  • Acute plaque change/rupture

Can also be due to:

  • Coronary artery vasospasm
  • Emboli (from left atrium-atrial fibrillation)
  • Vasculitis
  • Haematological abnormalities (sickle cell disease)
28
Q

What is a haemorrhage?

A

Extravasation of blood due to vessel rupture

29
Q

What might a haemorrage be due to?

A

Trauma or an intrinsit disease of a vessel

30
Q

Rupture of a major vessel causes accurate haemorrhage with risk of…?

A

Hypovolaemia, shock and death

31
Q

What is shock?

A

Systemic hypotension due to reduced circulatory volume or reduced cardiac output

32
Q

Name and describe 5 types of shock

A
  1. Cardiogenic shock
    • When the heart isn’t working properly
    • Numerous causes such as acute Mi, arrhythmias, cardiac tamponade etc.
  2. Hypovolaemic shock
    • Loss of blood or plasma due to haemorrhage or fluid loss
  3. Septic shock
    • An infection activates immune system
    • Resultatn vasodilation and pooling of blood
  4. Neurogenic shock
    • Loss of vascular tone
    • Cord injury, anaesthetic medication
  5. Anaphylatic shock
    • Allergic reaction
33
Q

What is the cause of hypovolaemic shock?

A
  • Fluid loss
  • Start having symptoms when more than 1L of blood (20%) is lost
34
Q

What is cardiogenic shock caused by?

A
  • Heart cannot pump enough blood to meet body’s demands
  • Caused by acute myocardial infarction
  • High mortality rate
35
Q

Outline the continuum from SIRS to septic shock

A
  1. Systemic inflammatory response syndrome (SIRS)
    • 2 or more of either:
      • Temperature >38 or <36°C
      • Tachycardia
      • High respiratory rate
      • High WBC count
  2. Sepsis (SIRS + infection)
  3. Severe sepsis
  4. Septic shock
36
Q

What is septic shock most commonly caused by?

A

Pathogen: gram positive bacteria

Endotoxins released by pathogens:

  • activate complement pathway
  • damage endothelial cells
  • tumour necrosis factor
37
Q

What are the general complications of a septic shock?

A
  • Organ dysfunction and multi-organ failure
  • Ischaemic tissue - lactic acidosis
  • Acute tubular necrosis

MCD - cell pathology (6 decks)

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