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Gen Pathology- PCCF tri 2 > hemodynamics - exam 2 > Flashcards

hemodynamics - exam 2 Flashcards

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1
Q

normal hemostasis

A

body’s natural way of stopping bleeding when blood vessel gets injured

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2
Q

What occurs in primary hemostasis?

A

Formation of initial platelet plug (weak)

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3
Q

What occurs in secondary hemostasis?

A

Formation of a stable clot through coagulation cascade

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4
Q

edema

A

accumulation of fluid in interstitial spaces/body cavities

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5
Q

causes of edema

A

Hydrostatic pressure, oncotic pressure, capillary permeability, lymphatic obstruction, sodium/water retention

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6
Q

examples of edema

A

congestive heart failure, nephrotic syndrome, liver cirrhosis, malnutrition, infection, burns, allergic reactions, filariasis, tumor compression, renal failure, hyperaldosteronism

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7
Q

localized edema

A

one area only

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8
Q

generalized edema

A

whole body swelling

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9
Q

pulmonary edema

A

fluid in the lungs

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10
Q

cerebral edema

A

brain swelling

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11
Q

ascites edema

A

fluid in peritoneal cavity

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12
Q

pleural effusion

A

fluid in pleural space

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13
Q

periorbital edema

A

puffy eyelids

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14
Q

examples of localized edema

A

exudates, deep vein thrombosis, lymphedema, + angioedema

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15
Q

examples of generalized edema

A

systemic renal fluid imbalance + hormone imbalance

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16
Q

hyperemia

A

active process of increased blood volume/flow

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17
Q

congestion

A

passive process, reduced outflow of blood

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18
Q

what is the cause of acute passive hyperemia

A

congestion

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19
Q

examples of acute passive hyperemia

A

varicose veins

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20
Q

what is the cause of active hyperemia

A

increased influx of arterial blood to an area

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21
Q

examples of active hyperemia

A

blushing

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22
Q

what is the cause of chronic passive hyperemia

A

congestion

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23
Q

example of chronic passive hyperemia

A

left ventricular failure

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24
Q

hemorrhage

A

Escape of blood from the circulatory system

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25
What are external causes of hemorrhage?
epistaxis, hemoptysis, hematesmesis, melena, hematuria, menorrhagia, metrorrhagia
26
epistaxis
Bleeding from the nose
27
hemoptysis
Coughing blood
28
hematesmesis
Vomiting blood
29
melena
Dark brown digested blood in stools
30
hematuria
Blood in urine
31
menorrhagia
Excessive menstrual blood
32
metrorrhagia
Uterine bleeding in between menstrual periods
33
What are internal causes of hemorrhage?
hemothorax, hemopericardium, hemarthrosis, hemoperitoneum
34
hemothorax
blood in pleural cavity
35
hemopericardium
blood in pericardial sac
36
hemarthrosis
blood in joint cavity
37
hemoperitoneum
blood in peritoneal cavity
38
hematoma
large amount of interstitial hemorrhage
39
petechiae
multiple small pinpoint lesions in skin caused by interstitial hemorrhage
40
purpura
slightly larger hemorrhages than petechiae, bleeding in skin
41
ecchymosis
moderate amount of interstitial hemorrhage
42
thrombosis
pathological formation of a blood clot within the vascular system
43
What are 3 causes of thrombosis?
vessel wall damage, blood flow disturbances, hypercoagulability
44
what is another name for the 3 causes of thrombosis
virchow's triad
45
Describe how a stable blot clot is formed from the 3 steps of the clotting cascade
tissue damage activated factor 3 + 4, > activates factor X. collagen/trauma activates factor xii > activates factor xi > activates factor ix + viii > activates factor x. factor x > activates prothrombin > activates thrombin > activates fibrinogen > activates fibrin > which cross links with factor xiii > forms a stable clot
46
turbulent blood flow
blood flow with eddy currents, platelets undergo shear stress
47
stasis blood flow
stagnant blood flow or no blood flow
48
laminar blood flow
normal blood flow
49
Explain how hypercoagulability leads to the formation of thrombus
A balance shift towards clot formation caused by changes in clotting factors, platelet activity, + natural anticoagulant system
50
What are common acquired causes of hypercoagulability?
Prolonged immobilization, pregnancy, cancer, oral contraceptives, smoking, myocardial infarction, fractures
51
Possible fates of a thrombus
Lysis, propagation, organization, recanalization, infection, embolization
52
Lysis
Complete removal by fibrinolytic activity
53
propagation
Extension of a clot
54
Organization
Ingrowth of granulation tissue
55
Recanalization
Reestablishment of lumen
56
Infection
Bacterial invasion
57
What are lines of zahn
Transverse whiteish lines in the vessels as the thrombus forms
58
What’re some clinical conditions that are related to thrombus formation?
Varicose veins, deep vein thrombosis, disseminated intravascular coagulation
59
Embolism
Detached intravascular solid/liquid/gas mass that is carried by blood to distant site from origin
60
What are the causes of emboli
Venous thrombi, arterial thrombi, paradoxical embolus, fat embolism, air, + amniotic fluid
61
Example of venous thrombi
Deep vein thrombosis
62
Paradoxical embolus
Ventricular septal defect
63
Fat embolism
Marrow in long bone fractures
64
Example of air cause of emboli
Caisson disease
65
examples of amniotic fluid causes of emboli
premature labor in late pregnancy
66
what are factors that increase risk of an embolism
type of thrombus, location, size, blood flow dynamics
67
infarction
area of ischemic necrosis caused by occlusion of arterial/venous drainage being impaired
68
what are causes of an infarction
thrombosis/embolism, local vasospasm, expansion of atheroma
69
how are infarction classified
red infarct + white infarct
70
red infarct characteristics
blockage of an end artery in kidney/spleen. aka hemorrhagic
71
white infarct characteristics
blockage of an artery in lung/liver. aka anemic
72
shock
a state with diminished cardiac output/reduced circulating blood volume, causing cellular hypoxia
73
what is shock characterized by
systemic hypoperfusion, reduced cardiac output, hypotension, tachycardia, sudden heart failure, severe allergies, sepsis
74
how is shock classified
non-progressive, progressive, + irreversible
75
non-progressive shock
vital organs, cardiac output, + blood pressure remain normal. body compensates for blood loss
76
progressive shock
compensatory mechanisms begin to fail
77
irreversible shock
survival is unlikely, cell necrosis
78
pathogenesis of shock
Loss of blood due to decreases cardiac output. Circulatory volume is inadequate, hypoperfusion results in ischemia
79
causes of shock
hypovolemic, cardiogenic, anaphylactic, neurogenic, spetic shock
80
anaphylactic pathogenesis
Rapid onset, mediators releases, increases mucous secretions, increased bronchial smooth muscle tone, bronchospasm, hypotension
81
neurogenic shock pathogenesis
Vasodilation, peripheral pooling of blood, hypovolemia, dilation, hypotension
82
septic shock pathogenesis
Endotoxin released, stimulated cytokines, create cytokine storm, cause vasodilation
83
which cytokines are involved in septic shock
interleukin-1, interleukin-6, interleukin-8, tumor necrosis factor
84
what are some effects of shock
Edema, acute respiratory distress syndrome, acute tubular necrosis, centrilobular necrosis, subendocardial infarction, myocardial dysfunction

Gen Pathology- PCCF tri 2 (6 decks)

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