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PATHOLOGY > CIRCULATORY DISTURBANCE > Flashcards

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
Q

major site of CHRONIC GENERAL PASSIVE HYPEREMIA

A

HEART & LUNGS

26
Q

the liver will show generalized
congestion and could result to necrosis of periacinar (or centrilobular) hepatocytes, in a characteristic gross appearance as “nutmeg liver”.

A

RIGHT SIDE CHF

27
Q

the lungs will show
severe congestion and edema, and in some, hydrothorax could be seen.

A

LEFT SIDE CHF

28
Q

The term hemorrhage obviously implies rupture of a blood vessel

A

HEMORRHAGE BY RHEXIS

29
Q

Yet, blood could also be lost from the blood vessels
through a passive process known as

A

HEMORRHAGE by DIAPEDESIS

30
Q

usual cause of hemorrhage, where blood vessels are
ruptured or a rant is created.

A

TRAUMA

31
Q

Deficiencies in blood coagulation factors
such as prothrombin following vitamin K deficiency and in liver disease cause a
condition called

A

HEMORRHAGIC DIATHESIS

32
Q

clinical significance of hemorrhage depends on:

A

location of hemorrhage
volume of blood lost
rate of blood lost

33
Q

is the formation of ante mortem clot within the blood vessels,

A

THROMBOSIS

34
Q

clot form is called

A

thrombus

35
Q

plural of thrombus

A

thrombi

36
Q

or the arrest of hemorrhage by clot formation involves five
essential steps:

A
  1. vascular contraction,
  2. stasis of blood,
  3. endothelial adhesion,
  4. blood coagulation, and
  5. platelet aggregation.
37
Q

This mechanism involves the components normally present in the plasma,

A

INTRINSIC CLOTTING FACTORS

38
Q

this mechanism that involves tissue component in
addition to the components from the blood.

A

EXTRINSIC CLOTTING FACTOR

39
Q

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

A

intrinsic & extrinsic clotting factors

40
Q

Central to both intrinsic and extrinsic pathways, its activation marks the point of convergence and initiation of the common pathway

A

Factor X (Stuart-Prower Factor):

41
Q

The end product of the coagulation cascade, it forms a clot by intertwining with blood cells, plugging the wound and stopping bleeding

A

FIBRIN

42
Q

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.

A

Glycocalyx Theory

43
Q

the negatively-charged surface of
endothelial lining lead to a mutual electrostatic repulsion between two sets
of negatively charged cells (endothelia and blood cells).

A

Surface Negativity Theory

44
Q

– 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.

A

Surveillance System Theory

45
Q

a prostaglandin that prevent platelet
aggregation by converting platelet aggregation factors (endoperoxidase
and thromboxane A2) into unstable substances.

A

prostacylin

45
Q

are three major determinants in the pathogenesis of thrombosis and are traditionally called the

A

Virchow’s triad

46
Q

Injury to the vessel wall triggers reactions involving endothelial cells, platelets, coagulation factors, and fibrin, leading to vasoconstriction and the formation of blood clots.

A

vascular damage

47
Q

alters blood rheology and favor thrombosis.

A

Venous stasis

48
Q

commonly known as serotonin

A

5-hydroxytryptamine

49
Q

norm blood pH is maintained between

A

7.35 and 7.45

50
Q

main buffer system

A

bicarbonate and carbonic acid.

51
Q

Excess of bicarbonate, or a deficiency of carbonic acid, leads to severe
alkylosis at a blood pH of about

A

7.8 pH

52
Q
A
52
Q

occurs following prolonged vomiting with loss of acid.

A

Metabolic alkylosis

52
Q
A

PATHOLOGY (23 decks)

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