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Cell pathology > Haemodynamic disorders > Flashcards

Haemodynamic disorders Flashcards

1
Q

What are the three forces involved in oedema?

A
  • capillary hydrostatic pressure
  • plasma oncotic pressure
  • tissue hydrostatic pressure
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2
Q

What are the causes of 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
  • Lymphatic Obstruction
    Lymphoedema - breast cancer treatment
    Filariasis can cause massive lymphatic obstruction
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3
Q

What is pulmonary oedema?
What is the cause?
What is the most common pathology?

A

Cause: Raised hydrostatic pressure in the pulmonary capillary bed

Most common pathology: Left ventricular failure causing increased pressure in the left atrium. This 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

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4
Q

What are the symptoms of pulmonary oedema?

A
  • Dyspnoea (worse when they lie flat - orthopnoea)

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

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5
Q

What are the four types of cerebral oedema and their causes?

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
Increase in sodium within cells encourages water to be taken up
Causes intracellular oedema
Common in ischaemic strokes

3) Osmotic - reduction in plasma osmolality
Cause: SIADH (Syndrome of Inappropriate ADH secretion)
SIADH is commonly caused by small lung cell carcinoma

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 moves into the interstitial space

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6
Q

Osmolality vs osmolarity

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 is anasarca

widespread accumulation of fluid in subcutaneous tissues and serous cavities (pitting)

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8
Q

What are the causes of generalised oedema?

A

Left Ventricular Failure - dependent oedema (accumulated in areas affected by gravity)

Nephrotic Syndrome - fluid accumulates in all parts of the body (causes reduced albumin)

Hepatic failure (causes reduced albumin so colloid pressure reduced)

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9
Q

How does heart failure cause oedema?

renin

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
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10
Q

What are the consequences of cerebral oedema?

A

leads to high intracranial pressure and so higher risk of brain herniation and death

to reduce this raise head, induce dehydration and surgical decompression

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11
Q

Which three things lead to the formation of a thrombus?

A

Virchow’s triad:
- change in blood flow (stasis) as during stasis platelets are exposed to endothelium and more likely to clot. Stasis an also cause thrombosis by changing the dilution of blood clotting factors.

  • change in endothelium e.g. damage or endothelium dysfunction
  • change to blood constituents e.g. hypercoagulability caused by genetics or acquired disorders
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12
Q

Cardiac thrombosis

A

E.g. 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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13
Q

Arterial thrombosis

A

Almost always related to vessel wall injury - often caused by atherosclerotic plaques
If artery narrows - ischaemia
occlusion - infarction

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14
Q

Venous thrombosis

A

Key factors: Stasis and Hypercoagulability
Most form in deep veins
Most important complication: Pulmonary Embolism

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15
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. Most are thromboemboli but can be air, fat, amniotic fluid or a tumour

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16
Q

Venous Thromboembolism

A

Most originate in Deep Veins

Most Significant Consequence - pulmonary (thrombo)embolism

17
Q

Pulmonary embolism and how do the consequences differ depending on where it gets lodged and its size?

A

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

Risk of death increases with time taken to make the diagnosis

18
Q

Cardiac thromboemboli

How does the location of lodging affect the outcome?

A

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

19
Q

What is are the causes of haemorrhages and what does the outcome depend on?

A

Causes:

  • Trauma
  • Intrinsic disease of the vessel

The result of a haemorrhage depends on:

  • Volume and rate of haemorrhage
  • Site
20
Q

What does the rupturing of a large and small vessel result in?

A

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

21
Q

What is the effect of a solid haematoma in the cranial cavity?

A

Formation of a solid haematoma within the cranial cavity can be fatal by causing a rise in intracranial pressure and tonsillar herniation

22
Q

What is shock and the most vulnerable organs?

A

Occurs when tissue perfusion is insufficient to meet metabolic requirements. Caused by pump failure or peripheral circulation failure.
Hypotension - circulatory collapse leading to ischaemia of multiple organs. Initially reversible.

Most Vulnerable Organs: Kidneys, Bowel, Brain, Lungs, Heart

23
Q

What are the five types of shock?

A
  • hypovolaemic
  • cardiogenic
  • septic
  • anaphylactic
  • neurogenic
24
Q

Hypovolaemic shock: causes and mechanism

A

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

25
Q

Cardiogenic shock: cause and mechanism

A

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

26
Q

Septic shock: cause and mechanism

A

Result of inflammatory response

Cause: Vasodilation

Reduced SVR –> Reduced MAP

27
Q

Anaphylactic shock: causes and mechanism

A

Result of IgE mediated hypersensitivity
Causes: Vasodilation, Increased Permeability

Reduced SVR –> Reduced MAP

28
Q

White and red infarcts and how do they heal?

A

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

29
Q

What is an infarction?

A

Tissue necrosis due to ischaemia.

Most due to obstruction of an artery

Some may occur due to venous obstruction

30
Q

What are the causes and consequences of MI infarctions?

A

causes: obstruction, vasospasm, compression
consequences: cardiac rupture, pericarditis

31
Q

What is SIRS?

A

systemtic inflammatory response syndrome - high/low temp, high/low WBC, tachycardia, respiratory rate high
DOESN’T MEAN THERE MUST BE AN INFECTION

32
Q

What is sepsis?

A

SIRS + response to an infection (infection identified by problems with organ function)

33
Q

What is severe sepsis?

A

sepsis + organ hypoperfusion

34
Q

What is septic shock?

A

severe sepsis and despite intervention there is still hypotension
will lead to multiple organ dysfunction syndrome unless treated (beyond stage of reversibility)

35
Q

Neurogenic shock: causes and mechanism

A

Cause: injury to sympathetic pathways
Normally happens after trauma
Mechanism: Widespread vasodilation and reduced SVR

36
Q

Two types of atherosclerotic plaques

A

Stable – thick fibrous cap, less likely to rupture

Unstable – thinner fibrous cap, more likely to rupture

37
Q

What is non cardiogenic pulmonary oedema?

A

Caused by increased permeability
ARDS – Acute Respiratory Distress Syndrome
Often caused by sepsis, shock and trauma

38
Q

What are the two types of MI?

A

Transmural – across the whole wall of the heart

Subendocardial – just the layer under the endocardium

39
Q

What are the four fates of a thrombus?

A

1) Propagation
Thrombus gets larger

2) Embolisation
Dislodges and travels to distant site

3) Dissolution
Thrombus is destroyed by fibrinolytics

4) Organisation and Recanalisation
As a result of the thrombus, there is inflammation
Thrombus becomes fibrotic and remodels
Lumen appears again allowing blood flow

Cell pathology (6 decks)

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