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Circulatory Disturbances > Circulatory Disturbances > Flashcards

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
Q

Is there equilibrium between the ISF and the blood capillary network?

A

yes

26
Q

What determines how/ when fluid leaks out of vessels?

A
  • proteins keep fluid in the intravascular space
  • these proteins exert an oncotic pressure to keep fluid intravascular.
  • plasma is high protein
27
Q

What are the 5 basic mechanisms that can disrupt fluid balance?

A
  1. Inc hydrostatic pressure
  2. Dec plasma oncotic pressure
  3. lymphatic obstruction
  4. Inc vascular permeability
  5. Na retention
28
Q

Define exudate vs. transudate

A

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
Q

Blood hydrostatic pressure

A

The pressure that the volume of blood within our circulatory system exerts on the walls of the blood vessels that contain it.

30
Q

What can increased hydrostatic pressure result in?

A
  • impaired venous outflow
    e. g. systemically = heart failure
    e. g. locally= thrombus/ tumor/ abscess/ torsion
31
Q

What can decreased plasma oncotic pressure result in ?

A

-oedema usually caused by hypoproteinanaemia

reduction in albumin causes decrease of plasma oncotic pressure allowing fluid to leak out

32
Q

What aetiological agents can elicit a decrease in plasma oncotic pressure?

A
  • parasites such as protein losing enteropathies -decreased production of albumin such as in liver disease/ malnutrition
33
Q

What can cause lymphatic obstruction?

A
  • physical damage
  • localised obstructions
  • (from trauma/ surgery/ inflammation/ neoplasia)
34
Q

Increased vascular permeability is caused by what and results in what?

A
  • inciting agents such as histamine.

- Causes high inflammation (high protein exudate)

35
Q

what mediates Hyperaemia?

A
  • vasoactive amines

- neurogenic mechanisms

36
Q

What is cyanosis

A

The blue-red colouration of congested tissue due to poor circulation or inadequate O2

37
Q

What are the main two forces determining how fluid moves between compartments?

A
  • vascular hydrostatic pressure

- plasma colloidal osmotic pressure

38
Q

What does normal haemostasis rely on?

A
  • platelets
  • endothelium
  • coagulation cascade
39
Q

What do platelets adhere to?

A

the sub endothelial collagen

40
Q

Adhesion of platelets to sub endothelial collagen stimulates what?

A
  • 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
Q

How does normal endothelium prevent coagulation? (3)

A
  1. acting as a mechanical barrier
  2. Having anti platelet and anticoagulant activities
  3. promoting fibrinolysis by activating plasminogen
42
Q

What are the 3 subcategories of bleeding disorders?

A
  1. clotting defects
  2. vessel disorders
  3. platelet disorders
43
Q

What is thrombosis?

A

The pathologic formation of a clot

44
Q

What are the 3 principle causes of thrombosis?

A
  1. endothelial injury
  2. disruption of blood flow
  3. Hypercoagulability
45
Q

How does injury to endothelial cells elicit bleeding disorders?

A
  • exposure of sub-endothelial collagen to blood

- initiates coagulation

46
Q

What are some pathways to injuring endothelial cells

A
  • trauma
  • metabolic disorders
  • invasion by worms etc.
47
Q

What is laminar flow?

A

ultimate/ optimum flow of blood

48
Q

How does disruption of blood flow catalyse circulatory disturbances?

A
  • Turbulence/ stasis encourages platelet contact with endothelial cells
  • Turbulence can damage endothelium
  • Result in coagulation/ thrombus
49
Q

What are the 4 steps in the outcome/ sequelae of thrombosis?

A
  1. Resolution due to fibrinolysis
  2. Organisation & recanalisaiton
  3. Embolism
  4. Infarction
50
Q

Describe “resolution due to fibrinolysis” as the first factor contributing to the outcome of a thrombus

A

Fibrinolysis acts to resolve a thrombus. It degrades the constituent fibrin to free/breakup the thrombus.

51
Q

If a thrombus cannot be resolved via fibrinolysis, what happens as the next step of resolution?

A

Organisation & recanalisation
* Capillary invasion *

  • vessels infiltrate to resume blood flow
  • initially the endothelial cells, followed by fibroblasts and smooth muscle cells.
52
Q

What is an occlusive thrombus?

A

one which obstructs the vessel lumen

53
Q

What is an obtrurating thrombus?

A

One which has a long free trailing end

54
Q

What is an infarct?

A

An area of ischaemic necrosis caused by the occlusion of the arterial supple or venous draining to a tissue.

55
Q

Why is infarction rare in tissues such as intestines?

A

They have good collateral circulation

56
Q

What is the difference between a thrombus and a blood clot?

A

Thrombi form in living animals

Blood clots form PM

57
Q

Do thrombi exhibit lamination?

A

Yes

Chronic thrombi exhibit laminations due to the layering effect

58
Q

Describe arterial vs. venous thrombi

A 
Arterial= dull, rough. 
Venous= Moist, gelatinous
59
Q

Are thrombi separated into red and yellow areas?

A

No, they are usually grey or pink.

Red and yellow “chicken fat clots” are PM blood clots.

60
Q

Are thrombi attached to a vessel wall?

A

Yes

61
Q

Are PM blood clots attached to a vessel wall?

A

No

Circulatory Disturbances (1 decks)

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