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Pathology I > Fluid And Hemodynamic Derangements > Flashcards

Fluid And Hemodynamic Derangements Flashcards

1
Q

excessive quantities of fluid that accumulate (typically) in the intercellular spaces

A

Edema

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2
Q

an “escape” of fluid into tissues or a structure
(as in movement of fluids from blood vessels into tissue
spaces or compartments)

A

Effusion (efflux)

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3
Q

TYpe of edema fluid that is a protein-poor fluid

consisting of water and electrolytes

A

Transudate

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4
Q

Type of edema fluid that is Protein-containing and results from leaky
(permeable) vessels

A

Exudate

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5
Q

Starlings hypothesis states that the direction and rate of movement of fluids between blood and the tissue spaces are influenced by:

A
  • Hydrostatic and osmotic pressures of blood
  • Hydrostatic and osmotic pressures of interstitial
    fluids
  • The properties of the vessel wall (filtering
    membrane)
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6
Q

The pathogenesis of edema occurs when there are alterations to Starling’s forces such as:

A
  • Increased hydrostatic pressure of venules and
    capillary beds, contributing causes include venous obstruction and pooling
  • Decreased oncotic (osmotic) pressure of plasma, Associated with hypoproteinemia
  • Increased vacular (endothelial) permeability - causes include injury, inflammation, hypoxia, some forms of shock etc.
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7
Q

Lymph obstructions can also cause edema. Where are some causes of lymph obstruction?

A
  • tumors
  • inflammation and scarring
  • elephantiasis
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8
Q

Excess peritoneal fluids

A

Ascites (hydroperitoneum)

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9
Q

Causes of ascites

A

Causes include chronic liver disease (most

common), CHF, and disseminated abdominal cancer

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10
Q

Excess pleural fluids

A

Hydrothorax (pleural effusion)

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11
Q

Causes of Hydrothorax (pleural effusion):

A

causes include “left side”

heart failure and obstruction of thoracic veins

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12
Q

severe generalized edema

A

Anasarca

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13
Q

Causes of anasarca:

A

contributing causes

include chronic congestive heart failure and renal disease

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14
Q

associated with subcutaneous edema,

applying pressure to the skin drives fluid out leaving a “dimple”

A

Pitting edema

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15
Q

fluids collect in “dependent region” of

body (ankle edema, etc.)

A

Dependent edema

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16
Q

What are local factor that contribute to edema?

A
  • venous obstruction
  • increased vascular permeability
  • lymphedema
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17
Q

What are some systemic factors that contribute to edema?

A
  • congestive heart failure

- hypoproteinemia

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18
Q

What are some common causes of venous obstruction that contributes to edema?

A

thrombi, tumors, poor posture,

tight garments, etc.

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19
Q

What are some possible causes of increased vascular permeability that would lead to edema?

A

inflammation,

vascular hypoxia, prolonged cold (“immersion foot)

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20
Q

HOw does congestive heart failure contribute to edema?

A

contributes to elevated

systemic venous pressure and reduced renal perfusion (renal hypoxia) with increased fluid retention

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21
Q

How does liver disease contribute to edema?

A

Liver disease leads to decreased synthesis of plasma proteins (hypoproteinemia) and fluid loss by osmosis

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22
Q

How does renal disease contribute to edema?

A

Can give rise to proteinuria and hypoalbuminemia when then leads to hypoproteinemia and fluid loss by osmosis

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23
Q

Is edema a disease?

A

No, it is a sign of disease

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24
Q

Organ edema with potential life threatening effects:

A
  • Pulmonary edema- alveolar spaces fill with fluid
  • Hydrothorax (pleural effusion) and
    hydropericardium may compress lungs or heart
  • cerebral edema - Swelling leads to compression and distortion of affected regions
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25
Q

localized excess of blood, engorgement

A

Hyperemia

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26
Q

Factors contributing to hyperemia

A
  • increased arterial blood flow (“active
    hyperemia”)
  • impaired venous drainage (“passive hyperemia”)
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27
Q

What causes passive hyperemia?

A

Impaired venous drainage and decreased outflow of blood from affected region; causes include heart failure, venous obstruction, etc.

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28
Q

What causes active hyperemia?

A

Increased arterial blood flow from exercise (increased blood flow in skeletal muscle) acute inflammation, temperature regulation, cutaneous blushing and responses to temporary interruption of blood supply. This type is regulated by neurogenic and hormonal influences

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29
Q

What kind of hyperemia is characterized by local redness and increased warmth?

A

Active hyperemia

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30
Q

What kind of hyperemia is characterized by cyanosis and edema?

A

Passive hyperemia because there is decreased outflow of blood from affected region

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31
Q

What is the effect of passive hyperemia in the lungs?

A
  • Pulmonary capillaries become engorged and leak fluid and blood cells
  • Hemosiderin containing macrophages accumulate and cause pulmonary fibrosis
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32
Q

What is the effect of passive hyperemia on the liver?

A

Centrilobular venous congestion leads to “nutmeg” liver (brown spots on pale background) and can eventually cause cirrhosis or necrosis. This can be due to CHF or obstruction of the hepatic veins/inferior vena cava

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33
Q

What is the effect of passive hyperemia on the spleen?

A

Portal venous congestion and hypertension will lead to distention of the spleen (splen omega LH) and engorgement of splenic sinuses

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34
Q

discharge of blood from vessels into surrounding tissues (“extravasation” of blood)

A

Hemorrhage

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35
Q

Loss of 20% of blood due to hemorrhage will result in:

A

Feeling sick

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36
Q

Loss of 40% of blood due to hemorrhage will result in:

A

Risk of hypovolemic shock

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37
Q

Chronic hemorrhage in which someone sustains losses of few ml/day of blood could give rise to ____.

A

Anemia

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38
Q

Discharge of blood from vessels to environment

A

External hemorrhage

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39
Q

Discharge of blood from vessels to tissue

A

Internal hemorrhage

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40
Q

What are the effects of internal hemorrhage on organs?

A
  • compression
  • destruction
  • disruption of blood supply
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41
Q

What are common causes of internal hemorrhage?

A
  • coagulation disturbances
  • platelet dysfunction
  • congestion
  • shock
  • vasculitis due to infection or hypersensitivity
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42
Q

Small, “pin-point” hemorrhages (1-2 mm) of epithelial tissues (skin, conjunctiva, mucous membranes, serosa, etc.)

A

Petechiae

Causes include shock, venous obstruction,
platelet abnormalities, etc.

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43
Q

Medium hemorrhagic patches (3-5

mm of epithelial tissues (skin, conjunctiva, mucous membranes, serosa, etc.)

A

Purpura

Causes include shock, venous obstruction,
platelet abnormalities, vasculitis, vascular degeneration or coagulation disorders

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44
Q

Large hemorrhagic patches (1-2 cm or more) of epithelial tissues (skin, conjunctiva, mucous membranes, serosa, etc.)

A

Ecchymosis (bruise)

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45
Q

Accumulation of blood in tissues that creates a

“mass”; in some instances, adjacent structures may be compressed

A

Hematoma

may affect local
blood flow and delay healing.

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46
Q

Bleeding into peritoneum

A

Hemoperitoneum

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47
Q

Bleeding in pleural spaces

A

Hemothorax

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48
Q

Bleeding into pericardium

A

Hemopericardium

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49
Q

Bleeding into joint space

A

Hemarthrosis

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50
Q

Respiratory bleeding

A

Hemoptysis

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51
Q

Bloody vomit

A

Hematemesis

52
Q

dark stool due to degraded blood pigment,

associated with bleeding in upper-mid GI tract

A

Melina

53
Q

“bright blood” present in stool, due to

bleeding in lower colon, rectum and anal regions

A

Hematochezia

54
Q

Causes of vascular obstruction

A
  • External compression: tumors, scar tissue
  • Arterial spasms
  • Diseases of vessel wall (arteriosclerosis and vasculitis) with narrowing, etc.
    4. Thrombi and emboli
55
Q

Closely regulated processes maintain blood in a fluid state under normal conditions and provide for rapid formation of localized hemostatic plugs at sites of vascular injury.

A

Hemostasis

56
Q

a pathological process that leads to the formation of aggregates of coagulated blood within the lumen of blood vessels or heart chambers in a living organism.

A

Thrombosis

57
Q

Arterial thrombosis is most commonly caused by:

A

atherosclerosis and
is a major cause of myocardial infarction, stroke and vascular obstruction of the lower extremities.

Other contributing causes include inflammatory
arteritis, aneurysms, and altered endothelial cell function

58
Q

a common complication of venous congestion (stasis), inflammation, trauma and hypercoagulability. They are most common in the deep veins of the lower extremities and pelvis

A

Venous thrombosis

DVT if in the deep veins of the lower extremity

59
Q

The Symptoms of DVT are variable but these thrombi carry a high risk for ____.

A

pulmonary embolization.

60
Q

coagulation of blood “everywhere else” except blood vessels and heart

A

Blood clots

61
Q

______ occur within blood vessels and heart

after death and are differentiated from antemortem thrombi.

A

Postmortem clots

62
Q

In general, activation of the ____ and ____ promote thrombosis

A

plasma clotting factors and platelets

63
Q

actions of the ____ and ____ inhibits this process.

A

endothelial cells and plasmin

64
Q

the circulating precursors
(clotting factors) are activated through a series of enzymatic interactions that ultimately give rise to thrombin and the polymerization of fibrinogen to form ____.

A

Fibrin

65
Q

hemostasis usually is associated with the _____ pathway of coagulation

A

intrinsic

66
Q

activation of the ____ pathway of coagulation is more common with thrombosis.

A

extrinsic

67
Q

What functions do platelets have in hemostasis?

A
  • formation of platelet plug
  • promote coagulation
  • produce thromboxane, ADP, growth factors and other agents
68
Q

Platelets are activated by exposure to collagen at site of injury and then undergo the following reactions:

A
  • adhesion
  • secretion
  • aggregation
69
Q

The _____ provides
molecular bridges between platelet surface receptors and exposed collagen in adhesion that are strong enough to overcome the hemodynamics forces of flowing blood

A

von Willebrand Factor

70
Q

Normal vascular endothelial cells exhibit antiplatelet, anticoagulant and fibrinolytic properties but when injured they also exert _____ actions. Ultimately, the balance between these activities determines whether thrombus formation, propagation or degradation occurs.

A

prothrombic

71
Q

Antiplatelet effects of normal vascular endothelial cells:

A

Normal endothelial cells are unreactive to non-activated platelets. These cells also secrete agents that inhibit platelet responses

72
Q

Anticoagulation effect of normal vascular endothelial cells:

A

Normal endothelial cells produce heparin-like agents and thrombomodulin which inactivate clotting factors

73
Q

Fibrinolytic properties of normal vascular endothelial cells

A

Normal endothelial cells synthesize plasminogen

activator which clears (degrades) fibrin deposits, etc.

74
Q

Procoagulant/prothrombic activities of injured vascular endothelial cells include:

A
  • Release of thromboplastin which
    activates the “extrinsic” pathway
  • Produce von Willebrand factor (vWF),
  • Inhibits plasminogen activator which diminishes fibrinolysis, etc.
  • Damage to the endothelium; collagen and other underlying elements are exposure to reactive elements of the blood
75
Q

Once activated, the thrombosis must be restricted (localized) to the site of origin to prevent coagulation of the entire circulatory system.
Regulatory and thrombolytic factors include the following:

A
  • Activation of serum protease inhibitors
  • “depletion” of local platelets and clotting factors
  • “Clearance” of activated factors by blood flow
  • Endothelial cell functions
  • Fibrinolytic mechanisms
76
Q

Describe the plasminogen system

A

activated plasmin lyses and removes fibrin clots; it also gives rise to “fibrin split products” which are weak anticoagulants. This is used in regulation of clotting

77
Q

How do streptokinase help regulate coagulation?

A

There are derived from certain bacteria and are used to lyse thrombi

78
Q

What is Virchow’s triad?

A

Predisposing factors that contribute to formation of thrombi

79
Q

What are the three predisposing factors of Virchow’s triad that contribute to formation of thrombi?

A
  • endothelial injury and dysfunction
  • alterations in blood flow
  • hypercoagulation
80
Q

dominant influence that may singly cause thrombosis:

A

Endothelial injury and dysfunction

81
Q

What are examples of endothelial injury and dysfunction that can contribute to formation of thrombi:

A
  • vascular lesions such as atherosclerosis and vasculitis

- Myocardial and valvular disease including cardiac dysfunction, endothelial injury and valve dysfunction

82
Q

What are examples of alterations in blood flow that could contribute to thrombi formation?

A
  • stasis due to vascular obstruction or immobilization, heart failure or other circulatory deficits
  • turbulence from aneurysms, valve lesions or atherosclerotic plaques
83
Q

Hypercoagulation “states” contribute less frequently to thrombosis but are also important causes; these include:

A 
- Tissue injury (trauma, surgery, burns) release
thromboplastins
- Obstetrical conditions
- Neoplasms 
- Smoking 
- Elevated estrogen 
- Polycythemia and other blood disorders
- Factor V mutations and other genetic factors.
84
Q

Thrombi formed in “moving blood”; are usually firmly attached to vessel wall

A

Antemortem thrombi

85
Q

Common locations from antemortem thrombi?

A

regions predisposed to

atherosclerosis, the heart and veins

86
Q

What are the classifications of antemortem thrombi?

A

Arterial (white) thrombi
Venous (red) thrombi
Septic (infected)
Bland (sterile)

87
Q

What are lines of Zahn?

A

alternating layers of fibrin and aggregated platelets as seen in arterial thrombi

88
Q

When are arterial thrombi occlusive and when are they usually non occlusive?

A

When formed in the aorta or within the heart, these are usually nonocclusive (mural) whereas occlusive thrombi are common in small arteries and in veins

89
Q

Are venous thrombi usually occlusive or not?

A

Occlusive

90
Q

Venous thrombi are usually associated with _____

A

Stasis

91
Q

Blood elements not associated to vessel wall that “settle out” and give rise to layer of “chicken fat” and “currant jelly”

A

Post Morten thrombi

92
Q

What does the “chicken fat” layer of a postmortem thrombi contain?

A

Lighter weight “supernatant portion” of platelets and fibrin

93
Q

What does the “currant jelly ” layer of a postmortem thrombi contain?

A

heavier elements enriched with RBC that “settle out”

94
Q

When thrombi enlarge and elongate

A

Propagation (extension)

Generally, propagation progresses in direction of blood
flow unless blood flow is blocked

95
Q

action of the fibrinolytic system commonly occurs 24-48 hours after thrombosis, especially in the lungs, and results in

A

Resolution (lysis)

96
Q

Thrombosis resulting in obstruction in sites remote to the location of the original thrombus

A

Embolization

97
Q

Abnormal masses carried in the blood, includes thrombi, gases,
lipids, amniotic fluid, tissue fragments, etc.

A

Emboli

99% of emboli are thrombo emboli

98
Q

What is a paradoxic emboli?

A

emboli of venous origin enter systemic

arteries through septal defects of heart or other abnormal arterial-venous connections

99
Q

Air- introduced in blood vessels through trauma
(laceration of veins, chest wall injury), vascular
catheterization, obstetric complications, injection and other procedures

A

Gas emboli

100
Q

nitrogen gas-bubbles form in the blood giving rise to pulmonary obstruction- ”chokes”) and in tissue (“bends”- with pain). May be encountered in underwater divers, high altitude flight crews, etc.

A

Rapid decompression

101
Q

What occurs with repeated compression/decompression exposure?

A

gas bubbles may accumulate and obstruct blood vessels in parts of the skeleton (known as “caisson disease”, etc.) and may cause ischemic necrosis of bone (head of femur, tibia and humerus, etc.).

102
Q

Said to be a ”distant” second to thrombi as a source of emboli

A

Soft tissue trauma and fracture of long bones contribute to fat and adipose emboli, these are carried through the systemic veins to reach the lungs

103
Q

disruption of blood supply leading to hypoxia and death (ischemic necrosis) of affected tissue

A

Infarct

104
Q

infarcts tend to be “______ -shaped” with the location of occlusion at the apex

A

wedge

105
Q

Causes of infarct

A

any form of cardiovascular inadequacy (CHF, shock, thrombi and emboli and any other interruption of blood flow)

106
Q

What kind of infarct is most common?

A

Arterial

Venous is less common except in single venous outlet such as gonads

107
Q

What is an anemic or ”pale” infarct

A

Type of infarct common in arterial obstruction of solid organs (heart, kidney spleen)

108
Q

What are predisposing risk factors for infarct?

A
  • Pre-existing cardiovascular disease
  • Low blood oxygen levels (anemia)
  • High oxygen requirements of affected tissues
  • Poor blood supply at the site of obstruction (collaterals help)
  • Acute onset and rapid progression of occlusive event (less time to adapt)
109
Q

Inadequate perfusion of tissues by blood leads to

A

Shock

110
Q

Shock due to loss of fluid

A

Hypovolemic shock

111
Q

What are causes of hypovolemic shock

A
  • hemorrhage
  • dehydration
  • inadequate water intake
  • excessive sweating
  • GI disturbance
112
Q

Inadequate perfusion of tissues by blood due to heart failing to pump

A

Cardiogenic shock

113
Q

What are some common causes of cardiogenic shock?

A

severe MI, fibrillation, valve rupture,

cardiac tamponade, large pulmonary embolus

114
Q

Loss of vasomotor tone (vasodilation) that can lead to shock

A

Peripheral pooling

-> pooling of blood -> decreased venous return -> decreased cardiac output -> inadequate perfusion of tissues

115
Q

Neurogenic causes of peripheral pooling that can lead to inadequate perfusion of tissues:

A
  • pain
  • deep anesthesia
  • brain or spinal cord injury
  • vasovagal syncope
116
Q

Type of shock associated with endotoxins proving bacterial infection

A

Septic shock

117
Q

TYpe of shock that is associated with sensitization to an antigen resulting in widespread vasodilation and bronchospasm

A

Anaphylaxis

118
Q

Clinical manifestations of shock:

A
  • cold skin (in hypovolemic and cardiogenic shock)
  • warm skin (in septic and anaphylactic shock)
  • Increased heart rate, weak pulse and sweating are common
  • hypoxia contributes to
    acidosis (anaerobic glycolysis gives rise to lactic acid) and increased risks for cell injury and death
119
Q

In early stages of shock ____ mechanism dominate and effects are reversible. Later, ____ may occur if not checked

A

Compensatory

Progressive shock

120
Q

What are the compensatory mechanisms for shock”

A
  • activation of SNS reflex for increased HR and peripheral vasoconstriction which helps maintain circulation in central organs but can cause ischemia in peripheral organs
  • secretion fo renin and angiotensin which elevates vasomotor tone and increases secretion of aldosterone to increase blood volume
121
Q

Severe or prolonged shock to the brain will cause:

A

Diminished CNS function due to “boundary zone” infarcts and global brain ischemia and necrosis

122
Q

Severe or prolonged shock to the heart will cause:

A

Greater risk of infarct due to poor oxygenation of blood, plus increased compensatory cardiac work load

123
Q

Severe or prolonged shock to the kidneys will cause:

A

renal tubular epithelium is at risk for necrosis during

severe or prolonged shock, this is known as ATN (acute tubular necrosis), which may cause acute renal failure

124
Q

Severe or prolonged shock to the lungs will cause:

A

widespread alveolar damage and respiratory failure (“shock lung”) may occur

  • the lungs are relatively unaffected by most forms of shock
    except septic shock
125
Q

Generally, all forms of shock may be considered to be reversible
but when advanced or with significant organ damage, shock may begin to ______.

A

decompensate

126
Q

What occurs when shock begins to decompensate when advanced and organ damage occurs?

A
  • The compensatory responses are no longer adequate or are reversed
  • Progressive vascular injury, damage to the vasomotor center and thrombosis contribute to deterioration and ultimately, irreversible changes
127
Q

What types of shock have the poorest prognosis?

A

Cardiogenic and septic

Pathology I (10 decks)

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