CIRCULATORY DISTURBANCE Flashcards

1
Q

distribution of fluid is a carefully controlled

A

HOMEOSTATIC MECHANISM

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2
Q

It play an important role in fluid distribution, hemostasis,
inflammation and healing.

A

ENDOTHELIAL CELLS

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3
Q

60% of the total lean body weight is composed of

A

WATER

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4
Q

40% of this is in the

A

INTRACELLULAR SPACE

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5
Q

15% in the

A

EXTRACELLULAR COMPARTMENT

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6
Q

5% in the

A

PLASMID

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7
Q

the accumulation of an excessive amount of extracellular water in the
interstitial fluid spaces

A

EDEMA

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8
Q

edema may be a:

A

TRANSUDATE or EXUDATE

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9
Q

The relationship between the various forces at work in the microcirculatory
bed is described by what is known as the

A

STARLING EQUILIBRIUM

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10
Q

balance exists between the?

A

NET FILTRATION & NET ABSORPTION PRESSURE

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11
Q

The changes associated with edema are dependent on:

A
  • the severity of edema
  • the rapidity of onset,
  • the extent,
  • the anatomic location, and
  • the underlying cause of edema.
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12
Q

often more evident in the:

A
  1. subcutaneous tissue,
  2. lungs
  3. brain.
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13
Q

– fixative of choice to retain edema lesion.

A

BOUINS FLUID

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14
Q

an inflammatory effusion or edema characterized
by, high protein content, increased specific gravity
& increased number of inflammatory cells

A

EXUDATE,

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15
Q

exudate is a type of ?

A

ACTIVE PROCESS

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16
Q

-a non-inflammatory effusion or edema
characterized by:
* Low protein content
* Low specific gravity
* Low or absence on inflammatory cells

A

TRANSUDATE

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17
Q

what type of process is transudate?

A

PASSIVE PROCESS

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18
Q

refers to a local increase in the volume of blood in
tissues due to dilation of the small blood vessels,

A

HYPEREMIA

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19
Q

occurs following an increase in demand for more blood as
in the stomach and intestines during digestion, in the stimulation of erectile
tissues, and in the fleeting and pleasing neurovascular dilatation called blushing.

A

PHYSIOLOGICAL HYPEREMIA

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20
Q

on the other hand occurs as a manifestation of some
alterations in blood flow characteristics. These
include those observed during inflammation, in cardiac failure, and obstructive
venous diseases.

A

PATHOLOGICAL HYPEREMIA

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21
Q

Three factors are considered in the classification of pathological hyperemia, and
includes the following:

A
  1. Duration of hyperemia (acute or chronic)
  2. Extent of hyperemia (general or local)
  3. The underlying mechanism (active or passive)
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22
Q

Occurs in inflammation, and is due to
engorgement of the vascular bed following an increase in arteriolar flow into the area. Characterized by bright color of tissue due to well oxygenated blood

A

Acute Local Active Hyperemia.

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23
Q

This refers to passive engorgement of
the drainage area due to obstruction in the venous drainage.

A

ACUTE LOCAL PASSIVE HYPEREMIA

24
Q

organ system develops chronic inflammatory lesions which progress to fibrosis and therefore, obstruction or impediment in the tissue’s venous drainage, chronic local passive hyperemia occurs.

A

CHRONIC GENERAL PASSIVE HYPEREMIA or
CONGESTIVE HEARTH FAILURE

25
major site of CHRONIC GENERAL PASSIVE HYPEREMIA
HEART & LUNGS
26
the liver will show generalized congestion and could result to necrosis of periacinar (or centrilobular) hepatocytes, in a characteristic gross appearance as “nutmeg liver”.
RIGHT SIDE CHF
27
the lungs will show severe congestion and edema, and in some, hydrothorax could be seen.
LEFT SIDE CHF
28
The term hemorrhage obviously implies rupture of a blood vessel
HEMORRHAGE BY RHEXIS
29
Yet, blood could also be lost from the blood vessels through a passive process known as
HEMORRHAGE by DIAPEDESIS
30
usual cause of hemorrhage, where blood vessels are ruptured or a rant is created.
TRAUMA
31
Deficiencies in blood coagulation factors such as prothrombin following vitamin K deficiency and in liver disease cause a condition called
HEMORRHAGIC DIATHESIS
32
clinical significance of hemorrhage depends on:
location of hemorrhage volume of blood lost rate of blood lost
33
is the formation of ante mortem clot within the blood vessels,
THROMBOSIS
34
clot form is called
thrombus
35
plural of thrombus
thrombi
36
or the arrest of hemorrhage by clot formation involves five essential steps:
1. vascular contraction, 2. stasis of blood, 3. endothelial adhesion, 4. blood coagulation, and 5. platelet aggregation.
37
This mechanism involves the components normally present in the plasma,
INTRINSIC CLOTTING FACTORS
38
this mechanism that involves tissue component in addition to the components from the blood.
EXTRINSIC CLOTTING FACTOR
39
These two systems have a pathway centering on the activation of Factor X (Stuart-Prower factor) into a common pathway that leads to fibrin formation
intrinsic & extrinsic clotting factors
40
Central to both intrinsic and extrinsic pathways, its activation marks the point of convergence and initiation of the common pathway
Factor X (Stuart-Prower Factor):
41
The end product of the coagulation cascade, it forms a clot by intertwining with blood cells, plugging the wound and stopping bleeding
FIBRIN
42
the non-thrombogenic properties of intact endothelial lining cells is due to the carbohydrate-rich cell coat (glycocalyx) that prevents circulating cells from adhering to the surface.
Glycocalyx Theory
43
the negatively-charged surface of endothelial lining lead to a mutual electrostatic repulsion between two sets of negatively charged cells (endothelia and blood cells).
Surface Negativity Theory
44
– Endothelial cells have the ability to synthesize prostacyclin (PGI2), a prostaglandin that prevent platelet aggregation by converting platelet aggregation factors (endoperoxidase and thromboxane A2) into unstable substances.
Surveillance System Theory
45
a prostaglandin that prevent platelet aggregation by converting platelet aggregation factors (endoperoxidase and thromboxane A2) into unstable substances.
prostacylin
45
are three major determinants in the pathogenesis of thrombosis and are traditionally called the
Virchow's triad
46
Injury to the vessel wall triggers reactions involving endothelial cells, platelets, coagulation factors, and fibrin, leading to vasoconstriction and the formation of blood clots.
vascular damage
47
alters blood rheology and favor thrombosis.
Venous stasis
48
commonly known as serotonin
5-hydroxytryptamine
49
norm blood pH is maintained between
7.35 and 7.45
50
main buffer system
bicarbonate and carbonic acid.
51
Excess of bicarbonate, or a deficiency of carbonic acid, leads to severe alkylosis at a blood pH of about
7.8 pH
52
52
occurs following prolonged vomiting with loss of acid.
Metabolic alkylosis
52