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Cell Pathology > Cell Pathology 1- Haemodynamic disorders > Flashcards

Cell Pathology 1- Haemodynamic disorders Flashcards

1
Q

What is Oedema

A

An abnormal increase in interstitial fluid.

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2
Q

What are the aetiologies of oedema

A
  1. Increased hydrostatic pressure
  2. Salt and H20 retention
  3. Reduced plasma oncotic pressure
  4. Inflammation
  5. Lymphatic obstruction
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3
Q

What percentage of the body weight does water constitute in both sexes

A
  • 60% of total body weight for men

- 50% total body weight for women

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4
Q

What are the two opposing forces acting on blood in the capillaries, describe the transport of substances in the capillaries

A

Opposing forces ; hydrostatic pressure and plasma oncotic pressure keep interstitial fluid in balance in the microcirculation.
Fluid leaves the circulation at the arterial end ( hydrostatic pressure> oncotic pressure)
Fluid enters the circulation at the venous end ( oncotic pressure > hydrostatic pressure)

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5
Q

What is the flow of interstitial fluid governed by

A

Flow of interstitial fluid is governed by 1) hydrostatic and oncotic pressures and 2) endothelial permeability

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6
Q

What is generalised oedema

A 
Fluid in serous cavities (pleural , pericardial, peritoneal) and subcutaneous tissues.
>5L
Causes:
Left heart failure
Inflammation
Venous hypertension
Lymphatic obstruction.
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7
Q

What is localised oedema

A 
Cerebral and pulmonary oedema
Causes:
Congestive heart failure
Hypoproteinaemia (low protein content)
 Nutritional oedema
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8
Q

Describe generalised pitting oedema

A

Widespread accumulation of fluid in subcutaneous tissues and serous cavities.

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9
Q

Describe how increased hydrostatic pressure can cause oedema

A

Heart failure results in increase in hydrostatic pressure (generalised oedema).

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10
Q

Describe how reduced plasma oncotic pressure (reduced albumin) can lead to oedema

A

Plasma oncotic pressure is governed by [albumin]
When [albumin] <25g/L fluid leaves the microcirculation
Cause of generalised oedema
Loss of protein ( nephrotic syndrome, protein loss enteropathy)

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11
Q

Describe how lymphatic obstruction can cause oedema

A

Localised oedema
Non pitting protein rich oedema
Obstruction by tumour, lymph node dissection, chronic inflammation

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12
Q

Describe how sodium retention can cause oedema

A

Reduced cardiac output ( volume of blood pumped out of the heart per unit time) stimulates the renin-angiotensin system which leads to sodium retention (generalised oedema).

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13
Q

Describe how inflammation can cause oedema

A

Loss of protein rich fluid locally

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14
Q

Describe the link between heart failure and systematic oedema

A

Reduced renal blood flow- activation of renal-angiotensin system to increase blood pressure again- can cause oedema due high hydrostatic blood pressure in patients with heart failure.

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15
Q

How does the renin-angiotensin system increase blood pressure

A

Drop in blood pressure and fluid volume
Renin release from kidney
Renin acts on angiotensinogen released from the liver, to form angiotensin 1
ACE (Angiotensin converting enzyme) is released from the lungs and converts angiotensin 1 into angiotensin 2.
Angiotensin 2 acts directly on blood vessels to stimulate vasoconstriction, as well as acting on the adrenal gland to stimulate the release of aldosterone, which increases the resorption of salt and water in the kidneys to increase blood pressure.

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16
Q

What are the causes of pulmonary oedema

A

Normally due to raised pulmonary capillary hydrostatic pressure, due to pulmonary venous congestion, of which a common cause is left ventricular failure,Fluid accumulates first in the interstitial space and then eventually spills into the alveolar spaces.
The consequences include breathlessness and pneumonia.

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17
Q

Explain the consequences of pulmonary oedema

A

Breathlessness (dyspnoea) is the main symptom.

Breathlessness is typically worse on lying flat (orthopnoea).

Fluid in the alveolar spaces predisposes to bacterial infection in the lung (pneumonia).

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18
Q

Describe the typical causes of cerebral oedema

A

Breakdown of normal capillary barrier and typically occurs in brain tissue surrounding lesions such as haemorrhages, infarcts, contusions and tumours. Cerebral oedema contributes to a rise in intracranial pressure, which can be fatal.
Vasogenic
Increased permeability of capillaries and venules
Cytotoxic
derangement of sodium-potassium membrane pump e.g. ischaemic strokes

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19
Q

Where can thromboses form

A

Veins, arteries and heart.

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20
Q

What is a thrombosis

A

Pathological clot formation in blood vessels (circulatory system) caused by abnormal activation of the haemostatic system.

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21
Q

Describe Vichow’s triad (the three factors that predispose thrombosis)

A

1) Endothelial injury
2) Stasis or turbulent blood flow
3) Blood hypercoagulability

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22
Q

How can endothelial injury lead to thrombosis

A

Endothelial injury leads to platelet activation

Arteries have high rates of blood flow and hence are under high shear stress; this leads to endothelial injury

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23
Q

How can a stasis or turbulent blood flow lead to thrombosis

A

Stasis and turbulent blood flow leads to endothelial injury
Stasis; disruption of laminar blood flow and development of venous thrombi
Turbulent blood; endothelial injury and formation of local pockets of stasis
Turbulent blood ;arterial and cardiac thrombi

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24
Q

How can blood hypercoagulability lead to thrombosis

A

Blood disorder that leads to thrombi formation
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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25
Q

Describe venous thrombosis

A

Usually related to stasis of blood and hypercoagulability.
Most form in deep leg veins (deep venous thrombosis or DVT).
Pulmonary embolism is the most important potential complication
Occlusive thrombi; due to sluggish blood flow
Composed of red blood cells >platelets
Can develop in healthy individuals with no risk factors
Veins of lower extremities mostly commonly affected
Venous thrombi have characteristic appearances with lines of Zahn (alternating layers of platelets and red blood cells)

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26
Q

Describe arterial thrombosis

A

Almost always related to vessel wall injury caused by atherosclerotic plaques.
Narrowing (stenosis) of the artery by thrombus causes ischaemia of the tissue supplied by the artery.
Complete blockage (occlusion) of the artery by thrombus causes infarction of the tissue supplied by the artery.
Occlusive thrombi composed of platelets, fibrin, red blood cells and leucocytes
Mostly in coronary > cerebral > femoral arteries
Most commonly superimposed on ruptured atherosclerotic plaques
Atherosclerosis leads to endothelial injury and abnormal blood flow

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27
Q

Describe cardiac thrombi

A

Stasis of blood in cardiac chamber-left atrium is associated with atrial fibrillation, left ventricle- myocardial infarct.

28
Q

What are the fates of thrombi

A

Propagation
Accumulation of further platelets and fibrin in a semi-occlusive thrombus
Embolisation
Thrombi can dislodge and travel through the circulation
Dissolution
Fibrinolysis in early thrombi; fibrinolytic agents ie t-PA
Organisation and recanalization
Older thrombi enveloped by fibroblasts, endothelial cells and smooth muscle cells
Capillary channels develop within the thrombus
These remain clinically silent, and can become significant if they occlude a vessel or embolize.

29
Q

What is meant by an embolus

A

An embolus is an abnormal detached mass within the circulatory system that is carried within the blood to a site distant from its point of origin. Most emboli (90%)are fragments of a dislodged thrombus (thrombo-emboli). Other types of emboli:
Vegetations ( from valves)
Gas ( interventional procedures, divers)
Fat ( fractures)
Tumour
Amniotic fluid ( childbirth)
Foreign material ( intravenous drug users)

30
Q

What can emboli cause

A

They can lodge in small vessels and occlude them.

31
Q

What may arise from a venous embolism

A

Venous emboli travel via the heart into the pulmonary arteries causing pulmonary embolism.

32
Q

What are the potential consequences of an arterial emboli

A

They may impact in cerebral arteries (causing stroke), the mesenteric arteries (causing small bowel infarction) or the lower limbs (causing acute lower limb ischaemia).

33
Q

Describe pulmonary embolism

A

Occlusion of pulmonary artery by embolus, which can cause instantaneous death if it occurs in a major pulmonary artery.Emboli lodging in medium sized arteries present with breathlessness.
Emboli lodging in small arteries cause subtle symptoms of breathlessness, chest pain, and dizziness – these are the hardest to diagnose- ‘silent’.
30% of patients with pulmonary embolism will die from it.
The risk of death increases the longer it takes to make the diagnosis.

34
Q

Describe systemic emboli

A

Arise in the arterial system
Originate from 1) dislodged atheromatous or 2)thrombi from within heart
Thrombi within the heart:
-due to cardiomyocyte death and thus no contractility- left ventricle
-due to atrial fibrillation- left atrium

Arterial emboli:
TIA (transient ischaemic attack), stroke, bowel infarction, limb ischaemia

35
Q

What is meant by an infarct

A

Tissue necrosis due to ischaemia
Most commonly caused by thrombotic or embolic vascular occlusion, though other causes need to be excluded
In occlusion of an artery either by thrombosis overlying a complicated atherosclerotic plaque or a thromboembolism (acute MI and cerebral infarction).
In venous obstruction the tissue becomes massively suffused with blood and appears dark purple or black (testicular torsion, sigmoid volvulus).

36
Q

Do infarcts normally heal

A

Infarcts heal by repair. Although structural integrity is maintained, there is permanent loss of functional tissue

37
Q

What are red infarcts

A

Occur as a result of venous occlusion
Occur in loose tissue; lungs
Occur in organs with dual circulation ; lung, bowel
Can reperfuse a site of previous arterial occlusion

38
Q

What are white infarcts

A

Occurs as a result of arterial occlusion

In dense/solid organs

39
Q

How can infarcts evolve over time and how are they shaped

A

Infarcts can be subtle initially and become more prominent with time.
They are wedge shaped.

40
Q

How does an infarcted segment of the small bowel appear

A

dark/dusky

41
Q

Describe myocardial infarction

A

Most commonly due to 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)

There is cardiomyocyte death

42
Q

Why is the diagnosis of myocardial infarction important

A

Myocardial Infarction can be reversible if treated early in most instances

43
Q

Describe the appearance of a myocardial infarction

A

Mottled areas ; acute Myocardial Infarction

White areas ; past Myocardial Infarction/ myocardial scarring

44
Q

Where do most pulmonary emboli originate from

A

DVT (lower extremities).

45
Q

What is meant by a haemorrhage

A

Extravasation of blood due to tissue rupture.

46
Q

What are the typical causes of a haemorrhage

A

May be due to trauma or an intrinsic disease of a vessel
Amyloid
Collagen vascular diseases
Rupture of a major vessel causes acute haemorrhage with risk of hypovolaemia, shock and death.
Examples include: Abdominal Aortic Aneurysm
Brain stem haemorrhage
Extravasation of blood due to vessel rupture
Even a small bleed at a vital site can be fatal- brainstem.

47
Q

What is hypovolaemia

A

Low volume of fluid in the blood.

48
Q

What are the typical symptoms of a ruptured abdominal aortic aneurysm.

A

back pain, hypotension and pulsatile mass

49
Q

What is meant by shock

A

Generalised failure of tissue perfusion. Systemic hypotension due to 1) reduced circulatory volume or 2)reduced cardiac output

50
Q

What are the typical causes of shock

A

Pump failure (acute MI) or peripheral circulation failure (hypovolaemia, sepsis, anaphylaxis) leading to circulatory collapse.

51
Q

List the different types of shock

A 
Hypovolaemic shock
Cardiogenic shock
Anaphylactic shock
Septic shock
Neurogenic shock
52
Q

Describe hypovolaemic shock

A

Loss of blood or plasma due to haemorrhage or fluid loss
>1L of blood (20%)
Most perfused organs: kidney, brain & skin

53
Q

Describe cardiogenic shock

A

Effectively the heart isn’t working properly ; numerous causes such as acute MI, arrhythmias, cardiac tamponade (compression of heart due to accumulation of fluid in pericardium). etc
Heart cannot pump enough blood to meet body’s demands
Caused by acute myocardial infarction
High mortality rate

54
Q

Describe septic shock

A 
An infection activates immune system ; resultant vasodilatation and pooling of blood
Systemic inflammatory response syndrome
>2 or more
Temperature >38 C or < 36 C
Tachycardia >90 bpm
Respiratory rare >20 breaths/min or PaCO2 <4.3KPa
WBC >12 x109/ L or >10% immature blasts
Sepsis
SIRS + infection
Severe sepsis
Sepsis + organ hypoperfusion

Septic shock
Severe sepsis + hypoperfusion despite adequate fluid resuscitation , or the use of vasopressors/inotropes to maintain blood pressure

55
Q

Describe neurogenic shock

A

Loss of vascular tone; cord injury, anaesthetic medication

56
Q

Describe the pathogens that may cause septic shock and the mechanisms that these pathogens use

A 
Pathogen: Gram positive > Gram negative bacteria > fungi
Endotoxins released by pathogens
Activate complement pathway
Damage endothelial cells
Tumour necrosis factor
57
Q

What are the complications of septic shock

A

Organ dysfunction and multi-organ failure
Ischemic tissue- Lactic acidosis
Acute tubular necrosis

58
Q

What are the typical signs of shock

A

The patient may look grey and clammy. There it tachycardia (rapid heart rate) and hypotension.

59
Q

What can untreated shocks lead to

A

Ischaemia of the heart, lungs, gut, kidneys and brain. Rapid treatment is necessary to prevent multiple organ failure and death.

60
Q

What is meant by atherosclerosis

A

An inflammatory disease of large and medium sized arteries characterised by the formation of lipid-rich plaques in the vessel wall.

61
Q

Describe the causes of atherosclerosis

A

Risk factors include: older age, male gender, obesity, diabetes mellitus, hypertension and smoking. Endothelial injury leads to an inflammatory and fibroproliferative response culminating in atherosclerosis.
Oxidised LDL is a potent driver.
Very common, particularly in developed countries.

62
Q

Describe the difference between stable and unstable plaques

A

Stable plaques cause symptoms of reversible ischaemia of the supplied organ- angina pectoris, chronic lower limb ischaemia.
Unstable (vulnerable) plaques can cause acute ischaemic events due to thrombosis overlaying them- acute coronary syndromes and cerebral infarction.

63
Q

How can fluid in the lungs be detected

A

Fine crackling

64
Q

Why do patients with pulmonary oedema need to lie down

A

Unable to breath lying flat- need an incline

65
Q

In which tissues does red infarct occur

A

Tissues with dual circulation such as the lungs.

66
Q

What are the risk factors of DVT

A 
Immobility
Surgery ( orthopaedic/ pelvic)
Trauma
Contraceptive pill; oestrogen
Thrombophilia
Malignancy
Obesity
Past DVT
Increased age
Pregnancy

Cell Pathology (6 decks)

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