5.4.1 Circulatory Disturbances

Question 1

Oedema

Answer 1

Abnormal accumulation of fluid within interstitial tissues

Question 2

What are the two types of oedema?

Answer 2

Non-inflammatory (low protein/cell) = transudate

Inflammatory (protein/cell rich) = exudate

Question 3

What are the four pathogeneses of oedema?

Answer 3

• ↑ intravascular hydrostatic pressue
• ↓ plasma osmotic pressue (loss/lack of albumin)
• ↑ capillary permeability (inflammatory origin)
• ↓ lymphatic drainage (inflammation/compression)

Question 4

What mechanism regulates blood pressure?

Answer 4

RAAS
Renin- Angiotensin- Aldosterone- System

Question 5

How does increase hydrostatic pressure result in oedema?

Answer 5

↑ blood volume in microvasculature = ↑ hydrostatic pressure

Generalised (systemic) due to RHS/LHS heart failure

Question 6

How does decreased osmotic pressure result in oedema?

Answer 6

↓ albumin = ↑ fluid filtration and ↓ absorption = generalised oedema

Hypoalbuminaemia - excessive loss or lack of production of albumin

Question 7

How does increased vascular permeability result in oedema?

Answer 7

Stimuli = vasodilation = ↑ permeability

Proteins escape into interstitial fluid = ↑ osmotic pressure = fluid drawn into intersitial fluid = oedema

Question 8

How does decreased lymphatic drainage result in oedema?

Answer 8

↓ drainage = ↑ fluid in interstitium - oedema

Question 9

Describe the morphology of oedema

Answer 9

Gross: clear-yellow gelatinous fluid

Histo: pale eosinophilic homogenous fluid

Question 10

What is hyperaemia

Answer 10

Active process of arterial dilation resulting in increased bloodflow = ↑ blood vol. in vessels

Question 11

What is congestion?

Answer 11

Passive process of decreased blood outflow from a tissue = ↑ blood vol. in vessels

Question 12

Pathology of hyperaemia

Answer 12

Occurs during early vascular response to inflammatory stimulus

Question 13

Physiology of hyperaemia

Answer 13

• Occurs during ↑ O2 demand
• Dissipation of heat
• Digestion of food

Question 14

Local vs generalised congestion

Answer 14

Local: obstruction/compression of venous outflow

Generalised: ↓ blood flow in heart/lungs = heart failure

Question 15

What does chronic congestion cause?

Answer 15

Lack of bloodflow = tissue hypoxia = ischemia and fibrosis

Question 16

Morphology of hyperaemia and congestion

Answer 16

Gross: H(bright red tissues), C(dark-red tissues)

Histo: dilation of blood vessels with RBCs

Question 17

What is shock?

Answer 17

Circulatory dyshomeostasis due to ↓ CO or ↓ circulating blood vol. and ↑ peripheral vascular resistance

Question 18

Three types of shock

Answer 18

Cardiogenic
- decreased stroke volume and output

Hypovolaemic
- decreased circulating BV

Blood maldistribution
- decreased effective circulating BV

Question 19

Cardiogenic stroke

Answer 19

failure of the heart to adequately pump blood

due to:
- myocardial damage
- arrhythmia
- compression
- outflow obstruction

Question 20

Hypovolaemic shock

Answer 20

reduced circulating blood

due to:
- haemorrhage
- fluid loss

Question 21

Blood maldistribution shock

Answer 21

reduced effective circulating BV

due to:
- neural/cytokine induced vasodilation
- septic / anaphylactic / neurogenic shock

Question 22

Three stages of shock

Answer 22

Nonpreogressive - reflex compensation mechanisms

Progressive - widespread tissue hypoxia

Irreversible - severe cellular / tissue damage

Question 23

Nonprogressive phase of shock

Answer 23

• Baroreceptors detect ↓ BP → epinephrine → ↑CO + vasoconstriction = ↑ vascular pressure
• ↓ plasma vol. → ADH release (RASS)→ vasoconstriction →↑ peripheral resistance

Question 24

Progressive phase of shock

Answer 24

• Intracellular aerobic resp. replaced by anaerobic resp. = excessive lactic acid = cellular and systemic acidosis
• metabolic acidosis ↓ tissue pH = blood pools
• ↓CO = endothelial cells risk hypoxic injury ∴ DIC

Question 25

Irreversible stage of shock

Answer 25

• O2 and energy stores depleted
• vital organs fail
• DIC