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Circulatory Disturbances Flashcards

1
Q

congestion

A

excess blood in vessels from low venous outflow

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2
Q

Congestive heart failure

A

congestion resultant of heart impediment

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3
Q

Hyperaemia

A

excess blood in vessels due to an ACTIVE engorgement in the vascular bed
-due to arteriolar dilation

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4
Q

Ischaemia

A

local reduction of blood supple to area due to obstruction/ vasoconstriction

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5
Q

Shock

A

blood supply to tissue becomes increasingly inadequate

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6
Q

Haemorrhage

A

escape of blood form vessels, either

  • diapedesis through intact walls
  • flow through ruptured walls
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7
Q

Haematoma

A

Circumscribed extravascular collection of blood

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8
Q

Give names of the events of haemorrhage into certain body cavities

A

Haemopericardium (into pericardium)
Haemoperitoneum (into peritoneum)
Haemothorax (into chest)
Haemothrosis (into joint)

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9
Q

Epitaxis

A

nose bleed

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10
Q

Haemoptysis

A

coughing up blood

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11
Q

Petechial haemorrhage

A

many “pin prick” haemorrhages

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12
Q

Thrombus

A

Blood clot in LIVING animal

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13
Q

Embolus

A

“matter” in the blood stream

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14
Q

Infarct

A

localised necrosis due to ischaemia

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15
Q

List the 5 mechanisms contributing to circulatory disturbances

A
  1. Hyperaemia & congestion
  2. Oedema
  3. Disorders of homeostasis (haemorrhage/thrombosis)
  4. Infarction & ischaemia
  5. Shock & fluid imbalances
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16
Q

What is the difference between hyperaemia and congestion

A

Hyperaemia is an ACTIVE process resulting from augmented BF via ARTERIAL DILATION
-Oxygenated blood

Congestion is a PASSIVE process resulting from impaired venous outflow.
-Deoxygenated blood

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17
Q

Hyperaemia is due to…

A
  • physiological events e.g. muscle due to exercise

- inflammation

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18
Q

Localised congestion can generally be attributed to…

A

a local obstruction

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19
Q

Hypostatic congestion can generally be attributed to…

A

gravity

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20
Q

Define oedema

A

is an abnormal accumulation of fluid in the interstitium, located beneath the skin and in the cavities of the body

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21
Q

What are some gross appearances of oedematous tissue

A
  • wet/ swollen
  • yellow/ clotted fluid
  • externally no redness
  • firm/ doughy consistency
  • pits on pressure
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22
Q

What are some microscopic appearances of oedematous tissue

A
  • inc intracellular space
  • protein count = high or low? –> stains pink or not?
  • chronic= organised & develops fibrous capsule
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23
Q

What is a cause of oedema

A

increased forces moving intravascular fluid to the interstitial space

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24
Q

What is the interstitium usually comprised of?

A
  • soluble gel in ECM

- insoluble fibres/ fibroblasts/ fibirils/ ECM (collagen and soluble gel)

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25
Is there equilibrium between the ISF and the blood capillary network?
yes
26
What determines how/ when fluid leaks out of vessels?
- proteins keep fluid in the intravascular space - these proteins exert an oncotic pressure to keep fluid intravascular. - plasma is high protein
27
What are the 5 basic mechanisms that can disrupt fluid balance?
1. Inc hydrostatic pressure 2. Dec plasma oncotic pressure 3. lymphatic obstruction 4. Inc vascular permeability 5. Na retention
28
Define exudate vs. transudate
Exudate= fluid exuded by the ACTIVE process of elimination from the intravascular space, because of injury or inflammation. Characteristically high in protein. Transudate: Any fluid (solvent and solute) that has passed through a presumably normal membrane, such as the capillary wall resultant of imbalanced hydrostatic and osmotic forces. characteristically low in protein.
29
Blood hydrostatic pressure
The pressure that the volume of blood within our circulatory system exerts on the walls of the blood vessels that contain it.
30
What can increased hydrostatic pressure result in?
- impaired venous outflow e. g. systemically = heart failure e. g. locally= thrombus/ tumor/ abscess/ torsion
31
What can decreased plasma oncotic pressure result in ?
-oedema usually caused by hypoproteinanaemia | reduction in albumin causes decrease of plasma oncotic pressure allowing fluid to leak out
32
What aetiological agents can elicit a decrease in plasma oncotic pressure?
- parasites such as protein losing enteropathies -decreased production of albumin such as in liver disease/ malnutrition
33
What can cause lymphatic obstruction?
- physical damage - localised obstructions - (from trauma/ surgery/ inflammation/ neoplasia)
34
Increased vascular permeability is caused by what and results in what?
- inciting agents such as histamine. | - Causes high inflammation (high protein exudate)
35
what mediates Hyperaemia?
- vasoactive amines | - neurogenic mechanisms
36
What is cyanosis
The blue-red colouration of congested tissue due to poor circulation or inadequate O2
37
What are the main two forces determining how fluid moves between compartments?
- vascular hydrostatic pressure | - plasma colloidal osmotic pressure
38
What does normal haemostasis rely on?
- platelets - endothelium - coagulation cascade
39
What do platelets adhere to?
the sub endothelial collagen
40
Adhesion of platelets to sub endothelial collagen stimulates what?
- Stimulates platelets to release cytoplasmic granules attracting more platelets which aggregate to form a plug - Stimilates coagulation cascade to produce fibrin to stabilize this plug
41
How does normal endothelium prevent coagulation? (3)
1. acting as a mechanical barrier 2. Having anti platelet and anticoagulant activities 3. promoting fibrinolysis by activating plasminogen
42
What are the 3 subcategories of bleeding disorders?
1. clotting defects 2. vessel disorders 3. platelet disorders
43
What is thrombosis?
The pathologic formation of a clot
44
What are the 3 principle causes of thrombosis?
1. endothelial injury 2. disruption of blood flow 3. Hypercoagulability
45
How does injury to endothelial cells elicit bleeding disorders?
- exposure of sub-endothelial collagen to blood | - initiates coagulation
46
What are some pathways to injuring endothelial cells
- trauma - metabolic disorders - invasion by worms etc.
47
What is laminar flow?
ultimate/ optimum flow of blood
48
How does disruption of blood flow catalyse circulatory disturbances?
- Turbulence/ stasis encourages platelet contact with endothelial cells - Turbulence can damage endothelium - Result in coagulation/ thrombus
49
What are the 4 steps in the outcome/ sequelae of thrombosis?
1. Resolution due to fibrinolysis 2. Organisation & recanalisaiton 3. Embolism 4. Infarction
50
Describe "resolution due to fibrinolysis" as the first factor contributing to the outcome of a thrombus
Fibrinolysis acts to resolve a thrombus. It degrades the constituent fibrin to free/breakup the thrombus.
51
If a thrombus cannot be resolved via fibrinolysis, what happens as the next step of resolution?
Organisation & recanalisation * Capillary invasion * - vessels infiltrate to resume blood flow - initially the endothelial cells, followed by fibroblasts and smooth muscle cells.
52
What is an occlusive thrombus?
one which obstructs the vessel lumen
53
What is an obtrurating thrombus?
One which has a long free trailing end
54
What is an infarct?
An area of ischaemic necrosis caused by the occlusion of the arterial supple or venous draining to a tissue.
55
Why is infarction rare in tissues such as intestines?
They have good collateral circulation
56
What is the difference between a thrombus and a blood clot?
Thrombi form in living animals Blood clots form PM
57
Do thrombi exhibit lamination?
Yes Chronic thrombi exhibit laminations due to the layering effect
58
Describe arterial vs. venous thrombi
``` Arterial= dull, rough. Venous= Moist, gelatinous ```
59
Are thrombi separated into red and yellow areas?
No, they are usually grey or pink. Red and yellow "chicken fat clots" are PM blood clots.
60
Are thrombi attached to a vessel wall?
Yes
61
Are PM blood clots attached to a vessel wall?
No

Circulatory Disturbances (1 decks)

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