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Pathology > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

EDEMA, HYPEREMIA AND HEMORRHAGE
symptoms (5)

A

-Tumor
-Rubor
-Calor
- Dolar
- Loss of function

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2
Q

Edema –

A

escape of fluid

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3
Q

Congestion –

A

Abnormal accumulation of blood

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4
Q

Infarction –

A

ischemic necrosis

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5
Q

Shock –

A

tissue injury secondary to systemic hypotension

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6
Q

Hemorrhage –

A

escape of whole blood

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7
Q

Thrombosis –

A

undesired clotting of blood

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8
Q

Embolism –

A

detached intravascular mass

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9
Q

Water accounts for –% of the lean body weight

A

60

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10
Q

Total body water is distributed between the

A

intracellular and extracellular compartments

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11
Q

Extracellular compartment
(2)

A

• Intravascular 5%
• Interstitial 15%

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12
Q

Hydrostatic Pressure

A

• Pressure exerted by volume of blood when confined
to a blood vessel

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13
Q

Osmotic (Oncotic) Pressure
(2)

A

• Proteins in blood vessels
• Albumin

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14
Q

Movement of Water Between the

A

Intravascular and Interstitial Spaces

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15
Q

Opposing effects of

A

vascular
hydrostatic pressure and
plasma colloid osmotic
pressure

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16
Q

Outflow at the arterial end
is nearly balanced by

A

inflow
at the venular end

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17
Q

Residual fluid left in the
interstitium is drained by

A

lymphatic vessels

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18
Q

— ml/min out

A

14

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19
Q

— ml/min in

A

12

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20
Q

— ml/min to
lymphatics

A

2

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21
Q

Increased hydrostatic pressure or decreased plasma osmotic pressure will cause

A

interstitial fluid to increase

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22
Q

If the capacity for lymphatic drainage is exceeded,

A

fluid accumulates (edema)

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23
Q

Edema -

A

swelling of tissues that result from excessive accumulation of fluid

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24
Q

Edema -
may be (3)

A

• May be highly localized as occurs in a small region of skin involved with an insect bite
• May be more regionalized, involving an entire limb or a specific organ, such as the lungs (e.g., pulmonary edema)
• May be generalized, involving the whole body

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25
Q

Hydrothorax

A

pleural effusion

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26
Q

Hydropericardium

A

pericardial effusion

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27
Q

Hydroperitoneum

A

ascites

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28
Q

Anasarca

A

generalized edema

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29
Q

Inflammatory causes of edema -

A

-inflammatory edema is caused by increased vascular permeability of a protein-rich exudate (exudate)

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30
Q

Non-inflammatory causes of edema -

A

edema caused by increased hydrostatic pressure or reduced oncotic pressure is usually protein-poor fluid (transudate)

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31
Q

Non-inflammatory causes of edema -
ex (4)

A

• Heart failure
• Renal failure
• Hepatic failure
• Malnutrition

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32
Q

Exudate –

A

high specific gravity – protein rich
• Inflammatory edema

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33
Q

Transudate –

A

low specific gravity – protein poor
• Volume or pressure overload
• Reduced plasma protein

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34
Q

Lymphangitis (2)

A

• Lymphatic spread of
bacterial infection
• Painful red streaks
and regional
lymphadenopathy

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35
Q

Lymphedema – (3)

A

a term used to describe an increase in
fluid in the interstitial space caused by an abnormality
in the lymphatic system
• Lymphatic fluid collects in tissues causing edema
• May be congenital or acquired

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36
Q

Acquired lymphedema
(2)

A

• Infection - filariasis
• Surgery, radiation therapy

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37
Q

Congenital Lymphedema - Aplasia

A

• Congenital malformation
of lymphatic system

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38
Q

Congenital Lymphedema - Aplasia
• Age 1 Week:

A

Lymphoscintigraphy exhibits
no migration of
radiopharmaceutical agent
from right foot to right
inguinal nodes

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39
Q

Congenital Lymphedema - Aplasia
• Diagnosis:

A

congenital aplasia
of the lymphatic system of
right leg

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40
Q

Congenital Lymphedema - Aplasia
Age 4.5 months:

A

debulked

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41
Q

Stewart-Treve Syndrome
(2)

A

• Angiosarcoma arising
from chronic
lymphedema
• Long-standing
lymphedema
secondary to surgical
lymph node dissection
and/or radiation
therapy

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42
Q

Anasarca in Renal Disease
(2)

A

• Severe
• Generalized edema

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43
Q

Edema Danger Zones (2)

A

• Lungs - Pulmonary edema
• Brain - Cerebral edema (central nervous system)

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44
Q

Cerebral Edema -
Cerebellar Tonsil Herniation (2)

A

• Increased intra-cranial pressure may result in herniation through the foramen magnum
• Compression of the medulla results in depression of the centers for respiration and cardiac rhythm control

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45
Q

Localized edema is usually caused by
(2)

A

• Increased vascular permeability (injury-inflammation)
• Obstruction of venous or lymphatic outflow

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46
Q

Generalized edema is generally caused by

A

decreased
plasma osmotic pressure

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47
Q

Increased hydrostatic pressure -
def
ex (2)

A

impaired venous return
• Congestive heart failure
• Venous obstruction or compression

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48
Q

Decreased plasma osmotic pressure (hypoproteinemia)
(3)

A

• Protein-losing glomerulopathies (nephrotic syndrome)
• Liver cirrhosis (ascites)
• Protein malnutrition

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49
Q

Lymphatic obstruction
(4)

A

• Inflammatory
• Neoplastic
• Postsurgical
• Postirradiation

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50
Q

Sodium retention
(4)

A

• Excessive salt intake with renal insufficiency
• Increased tubular reabsorption of sodium
- Renal hypoperfusion
- Increased renin-angiotensin-aldosterone secretion

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51
Q

Inflammation

A

increased permeability

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52
Q

Hyperemia

A

An active process in which
arteriolar dilation leads to
increased blood flow
• Sites of inflammation
• Skeletal muscle during
exercise

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53
Q

Hyperemia
Affected tissues turn red
(erythema) because of

A

engorgement of vessels with
oxygenatged blood

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54
Q

Congestion –
Deep Venous Thrombosis
(3)

A

• A passive process resulting from
reduced outflow of blood from a tissue
(stasis)
• May be systemic (heart failure) or
local (isolated venous obstruction)
• Congested tissues take on a dusky,
reddish-blue color (cyanosis) due to
red cell stasis and accumulation of
deoxygenated hemoglobin

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55
Q

Nutmeg Liver

A

Chronic Passive Congestion of Liver

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56
Q

Superior Vena Cava Syndrome

A

Compression of
superior vena cava
by neoplasm
obstructing venous
return

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57
Q

Hemorrhage –

A

extravasation of blood into the extravascular space

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58
Q

Capillary bleeding

A

oozing

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59
Q

Venous hemorrhage

A

seeping

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60
Q

Arterial hemorrhage

A

pulsating

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61
Q

Severe hemorrhage

A

rupture of a large vessel secondary to injury

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62
Q

Severe hemorrhage
ex (3)

A

Trauma, atherosclerosis, erosion of a vessel wall (inflammation or neoplasia)

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63
Q

Hemorrhagic diathesis –

A

increased tendency to hemorrhage occurs in a
variety of clinical disorders collectively called hemorrhagic diatheses

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64
Q

Hemothorax

A

thoracic cavity

65
Q

Hemopericardium

A

pericardial cavity - cardiac
tamponade

66
Q

Hemoperitoneum

A

peritoneal cavity

67
Q

Hemarthrosis

A

joints

68
Q

Petechiae

A

pinpoint hemorrhages

69
Q

Purpura

A

petechiae become
confluent

70
Q

Ecchymosis

A

purpurae become
confluent

71
Q

Hematoma

A

cavity

72
Q

Hemoglobin

A

red-blue

73
Q

Biliverdin

A

yellow-green

74
Q

Bilirubin

A

green-brown

75
Q

Hemosiderin

A

golden yellow

76
Q

Site of hemorrhage

A

• Subcutaneous tissues vs brain

77
Q

Volume and rate of hemorrhage
• Rapid loss of up to —% of blood
volume, or slow losses of larger
amounts may have little impact on
healthy adults
• Greater losses may cause

A

20
hemorrhagic (hypovolemic) shock

78
Q

Immune Thrombocytopenic Purpura (ITP) (2)

A

• Autoimmune disease–
antiplatelet
autoantibodies produce
thrombocytopenia
• Treatment with
steroids, splenectomy

79
Q

Hemostasis –

A

a physiologic process that maintains blood in a fluid state in normal vessels, yet also permits the rapid formation of a hemostatic clot at the site of a vascular injury

80
Q

Thrombosis –

A

pathologic counterpart of hemostasis that involves blood clot

81
Q

Hemostasis and Thrombosis
Both involve three components

A

• Vascular wall (endothelium)
• Platelets
• Coagulation cascade

82
Q

von Willebrand Disease (5)

A

Most common hereditary bleeding disorder
• Group of bleeding disorders
• Quantitative or qualitative abnormality of
the von Willebrand factor (vWF)
• vWFis required for normal platelet
adhesion
• vWF is the carrier protein for factor VIII

83
Q

vWF has functions in both

A

primary and secondary hemostasis

84
Q

Primary hemostasis – vWF:
(2)

A

• Attaches to platelets via a receptor for glycoprotein Ib on the platelet surface
• Acts as a bridge between the platelets and damaged subendothelium at the site of vascular injury

85
Q

Secondary hemostasis – vWF:
(2)

A

• Protects factor VIII from degradation
• Delivers factor VIII to the site of injury

86
Q

von Willebrand Disease (2)

A

• Normal platelet count with increased bleeding time
• Compound defect involving platelet function and coagulation pathway

87
Q

Factors Favoring Thrombosis (Virchow’s Triad)

A

• Endothelial injury
• Stasis or turbulent blood flow
• Hypercoagulability of the blood

88
Q

• Balance between antithrombotic and prothrombotic properties of endothelium determines

A

whether thrombus formation, propagation or dissolution occurs

89
Q

Normally, endothelial cells exhibit (3) properties

A

antiplatelet, anticoagulant and antifibrinolytic

90
Q

Endothelial cells may be activated by (5)

A

trauma,
infectious agents,
hemodynamic forces,
plasma mediators and
cytokines

91
Q

After activation, endothelial cells acquire

A

procoagulant activities

92
Q

• Mural thrombi

A

• Occur in heart chambers or aortic lumen

93
Q

• Arterial thrombi
(3)

A

• Frequently occlusive
• Coronary, cerebral, femoral arteries, most commonly
• Superimposed on ruptured, ulcerated atherosclerotic plaque

94
Q

• Venous thrombi
(2)

A

• Usually occlusive – thrombus forms a long cast of the lumen
• Veins of lower extremities

95
Q

• Vegetations –

A

thrombi on heart valves

96
Q

Thrombi are focally
attached to the

A

underlying
vascular surface

97
Q

Thrombi propagate from

A

the point of attachment in
the direction of blood flow

98
Q

The propagating portion
of a thrombus is often
poorly attached and is
prone to

A

fragmentation
and embolization

99
Q

Arterial or cardiac thrombi
(2)

A

• Begin at sites of turbulence or endothelial injury
• Propagate away from the heart

100
Q

Venous thrombi
(2)

A

• Occur at site of stasis
• Propagate toward the heart

101
Q

Lines of Zahn (4)

A

• Thrombi often have groosly and microscopically apparent laminations called lines of Zahn
• Pale platelet and fibrin deposits alternating with darker red cell-rich layers
• Laminations signify that a thrombus has formed in flowing blood
• Their presence can therefore distinguish antemortem thrombosis from the bland, non-laminated clots that occur postmortem

102
Q

Fate of a Thrombus (4)

A

Dissolution
Propagation
Embolization
Organization and recannalization

103
Q

• Dissolution –

A

fibrinolysis (plasmin)

104
Q

• Propagation –

A

accumulate additional platelets and fibrin

105
Q

• Embolization –

A

dislodge and travel to other sites in the vasculature

106
Q

• Organization and recannalization
(2)

A

• Ingrowth of endothelial cells, smooth muscle cells and fibroblasts
• Capillary channels eventually form that re-establish the continuity of the original lumen to a variable degree

107
Q

Clinical Consequences of Thrombi (2)

A

• Obstruct veins and arteries
• Embolize downstream

108
Q

Venous thrombi (phlebothrombosis)
(2)

A

• Congestion and edema in vascular beds distal to the obstruction
• Embolize to lungs and cause death

109
Q

Arterial thrombi
(2)

A

• Thrombotic occlusions at critical sites (stroke, myocardial infarct)
• Embolize and cause downstream infarctions

110
Q

Most venous thrombi occur in

A

superficial or deep veins of lower extremity

111
Q

Superficial venous thrombi
(2)

A

• Cause local congestion, swelling, pain and tenderness
• Rarely embolize

112
Q

Deep venous thrombi (DVT)
(3)

A

• Cause local pain and edema – rapidly offset by collateral channels
• More often embolize to lungs
• Half are asymptomatic, recognized in retrospect after embolization
15

113
Q

Risk Factors for Venous Thrombi (7)

A

• Hypercoagulable states
• Endothelial injury
• Bedrest, immobilization
• Congestive heart failure
• Trauma, surgery, burns
• Thrombotic diathesis of pregnancy
Neoplasia

114
Q

Risk Factors for Arterial
and Cardiac Thrombi (3)

A

• Cardiac and aortic mural thrombi may embolize
peripherally and cause infarcts of brain, kidney and spleen
• Major cause of arterial thrombi is atherosclerosis
• Predisposition to cardiac thrombi associated with
• Myocardial infarct
• Rheumatic heart disease
• Atrial fibrillation

115
Q

Disseminated Intravascular
Coagulation (DIC)

A

• Formation of widespread fibrin thrombi in the microcirculation
• Thrombi not grossly visible – can be seen microscopically
• May cause diffuse circulatory insufficiency, especially in brain,
heart, lungs and kidneys
• Widespread microvascular thrombosis results in platelet and
coagulation protein consumption (consumptive coagulopathy)
• Fibrinolytic mechanisms are activated
• The initially thrombotic disorder may evolve into a bleeding
disorder
• Not a primary disease but a potential complication of any
condition associated with widespread activation of thrombin
• Obstetric complication
• Advanced malignancy

116
Q

Embolus

A

A detached intravascular solid, liquid or gaseous
mass that is carried by the blood to a site distant
from its point of origin

117
Q

Embolus
Lodge in vessels…

A

too small to permit further
passage and cause partial or complete occlusion

118
Q

Embolus
Major consequence is

A

ischemic necrosis (infarction) of
the downstream tissue

119
Q

Thromboembolus –

A

almost all emboli represent
some detached part of a thrombus

120
Q

Venous emboli –

A

tend to lodge in one vascular bed (lung)

121
Q

• Arterial emboli –

A

can travel to a wide variety of sites

122
Q

Arterial emboli
Point of arrest depends on (2)

A

source and relative amount of blood flow

123
Q

Arterial emboli
Major sites are

A

Major sites are lower extremities and brain

124
Q

Arterial emboli
Consequences depend on

A

vulnerability of tissue to ischemia, caliber of occluded vessel and collateral blood supply

125
Q

Paradoxical Embolus

A

An embolus that originates on the right
side venous circulation and lodges in
the left side systemic arterial
circulation

126
Q

• Thromboemboli –

A

most emboli are thromboembolic in origin

127
Q

• Fat -

A

bone fractures

128
Q

• Bone marrow -

A

bone fractures

129
Q

• Air -

A
130
Q

• Nitrogen bubbles –

A

decompression sickness in divers caisson disease

131
Q

• Atherosclerotic debris (cholesterol emboli) -

A
132
Q

• Tumor fragments -

A
133
Q

• Amniotic fluid –

A

obstetric complication

134
Q

• Foreign bodies –

A

catheters, etc.

135
Q

• Infarct -

A

an area of ischemic necrosis caused by occlusion the
vasculature

136
Q

• Most infarcts occur from

A

thrombotic or embolic arterial
occlusions

137
Q

• Venous thrombosis may cause

A

infarction, but usually just
congestion

138
Q

• Atherosclerotic vascular disease causes

A

40% of all deaths in the
United States – mostly myocardial infarction or cerebral
infarction

139
Q

Ischemia
(2)

A

• Restriction in blood supply, usually due to factors in
the blood vessels
• Oxygen, glucose and other blood-borne materials

140
Q

• Infarct
(2)

A

• Complete loss of blood supply, resulting in necrosis
• An area of ischemic necrosis

141
Q

• Hypoxia
(2)

A

• More general term denoting a shortage of oxygen
• Usually a result of lack of oxygen in the air being
breathed

142
Q

Factors that Influence Development of an Infarct
(4)

A

Nature of the vascular supply – single vs double
Rate of occlusion development
Vulnerability of individual tissue to hypoxia
Amount of oxygen in the blood – anemia or cyanosis

143
Q

Nature of the vascular supply – single vs double
(3)

A

• Lungs – dual pulmonary artery and bronchial artery
blood supply
• Liver – dual hepatic artery and portal vein circulation
• Kidney and spleen circulations are end-arterial

144
Q

Rate of occlusion development

A

• Slowly-developing occlusions provide time to develop
alternate perfusion pathways – collateral circulation

145
Q

Vulnerability of individual tissue to hypoxia
• Neurons –
• Cardiac myocytes –
• Fibroblasts -

A

3 to 4 minutes
20 to 30 minutes
hours

146
Q

Insufficient blood supply is the most common cause of

A

gangrene

147
Q

types of gangrene

A

• Ischemic gangrene (dry gangrene)
• Infectious gangrene (wet gangrene)

148
Q

gangrene
Often associated with

A

peripheral vascular disease secondary to diabetes and long-term smoking

149
Q

Thrombophlebitis -
Phlebothrombosis (2)

A

• Superficial veins
• Deep leg veins – high risk
of pulmonary embolus

150
Q

Trousseau Syndrome (4)

A

• Migratory thrombophlebitis
• Paraneoplastic syndrome
• Hypercoagulability
• Adenocarcinoma
• Pancreas
• Colon
• Lung

151
Q

Shock

A

Systemic hypotension due to either reduced
cardiac output or to reduced effective
circulating blood volume

152
Q

shock leads to

A

impaired tissue perfusion and
cellular hypoxia

153
Q

shock
Initially — cellular injury

A

reversible

154
Q

Prolonged shock leads to

A

irreversible cellular
injury

155
Q

Cardiogenic shock –

A

low cardiac output due to pump
failure

156
Q

Causes of Shock (4)

A

• Myocardial infarct
• Ventricular arrythmias
• Extrinsic compression (cardiac tamponade)
• Outflow obstruction (pulmonary embolism)

157
Q

Hypovolemic shock –
def
ex (2)

A

low cardiac output due to loss of
blood or plasma volume
• Massive hemorrhage
• Fluid loss from severe burns

158
Q

Septic shock –

A

vasodilation and peripheral pooling of blood
as part of a systemic immune reaction to a bacterial or
fungal infection

Pathology (23 decks)

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